Pathophysiology: Total Questions-2020 General Pathophysiology: 1448 Special Fiztiopatologia: 572

PATHOPHYSIOLOGY:
Total questions-2020
General pathophysiology: 1448
Special Fiztiopatologia: 572
PATHOPHYSIOLOGY -GENERAL
1. NOZOLOGIA (62)
1. What is the General etiology?

1. the fiziopatologiei study of the causes of diseases and conditions
2. bin fiziopatologiei who study the causes of disease
3. the fiziopatologiei studying conditions of bolior
4. fiziopatologiei compartment that is studying the mechanisms of evolution
5. fiziopatologiei compartment that is studying the mechanisms of disease evolution
(1)
2. (5) The endogenous question serves as a factor of the disease?

1. changing the pH of the blood
2. pathogenic strain of e. coli from the gut
3. ascaride infestation
4. gene mutations that appeared on lifetime under the action of ionizing radiation
5. gene mutations inherited from predecessors
3. (1) what are the necessary conditions for the emergence of the disease?
1. various forms of substances, energy and information
2. biological field generated by other people
3. telepathic influence submitted by others
4. alien influences
5. electrical and magnetic fields generated by other living beings
4. (2) what effect exercise conditions favourable for the body?

1. fosters the emergence of disease cause and action
2. increase the body's resistance to harmful factors
3. reduces the body's resistance to harmful factors
4. decrease the reactivity of the organism from the harmful factor action
5. aura purifies and biocâmpul body
5. (3) what effect exercise conditions unfavorable for the body?

1. prevents the occurrence of disease cause and action
2. prevent the action cause and retains the appearance of the disease
3. reduces the body's resistance
4. increases the body's resistance
5. aura purifies and biocâmpul body
6. What are the conditions that influence the occurrence of endogenous disease?
1. ecological factors
2. climatic factors
3. microclimaterici factors
4. psychological microclimate in the family and working groups
5. the Constitution, the reactivity and the body's resistance
(5)
7. What is the General pathogenesis?

1. the fiziopatologiei studying the laws of occurrence, evolution and disease resolution
2. the fiziopatologiei studying the laws of development of pathological processes and disease
3. the fiziopatologiei study of the resolution of general laws
4. the fiziopatologiei studying the laws of originei diseases
5. the fiziopatologiei studying the laws of occurrence, evolution and resolution of each
disease
(1)
8. (2) what is the role of cause in the occurrence of disease?

1. determines the duration of illness
2. determine the specifics of the disease
3. when the disease detremină
4. determines the complications of the disease
5. determines the prognosis of the disease
9. (4) what is the role of conditions in the appearance of the disease?

1. determines the duration of illness
2. determine the specifics of the disease
3. when the disease detremină
4. prevent or accelerate the occurrence of the disease
5. determines the specific symptomatic disease
10. (5) what is the role of cause in the evolution of the disease?
1. in all diseases cause plays a role, and then trigger the disease develops under its own laws
2. in all diseases cause has decisive role throughout the disease causing all her manifestations
3. in all diseases cause has decisive role only in some periods
4. in all diseases cause different role in acute and chronic forms of the disease
5. in the presence of some diseases cause is needed throughout, from the onset to resolution
1. only in some diseases cause can also trigger, then disease develops under its own laws
2. in all diseases cause can have a decisive role throughout the disease causing all her
manifestations
3. the cause of all diseases may be present throughout the illness and her role can be decisive
in some stages and low in other stages
4. the cause of all diseases can have different role in acute and chronic forms of the disease
5. in the presence of all diseases is needed throughout, from the onset to resolution
1. the cause of all diseases can also trigger, then disease develops under its own laws
manifestations
3. in some diseases cause may be present throughout the illness and her role can be decisive
manifestations
8. in some diseases cause may be present throughout the illness and her role can be decisive
11. in some diseases cause can also trigger, then disease develops under its own laws
manifestations
15. (4) what is the lesion?

1. dishomeostazii persistent functional at any level of organization of the body
2. persistent structural dishomeostazii at any level of organization of the body
3. dishomeostazii persistent biochemical changes at every level of the Organization
4. dishomeostazii persistent structural, biochemical and functional at any level of
organization of the body
5. persistent energy dishomeostazii at any level of organization of the body
16. (3) Which is the possible combination of General and local lesions in the disease?
1. in all diseases injuries wearing exclusive local character

2. in all diseases injuries wearing exclusive general character
3. all diseases are a combination of local and General injuries
4. all diseases begin with General injuries and later appear and local lesions
5. all diseases first begins with local lesions, and subsequently appear and General
injuries
17. (3) Which is the combination of General and local lesions in the disease?
1. some diseases will result with injuries in the exclusive locale and others with injuries in
general exclusive
2. all diseases first begins with local lesions and later appear and General injuries
3. some diseases begin with local lesions, and subsequently appear and General injuries
5. all diseases first begins with local lesions, and subsequently appear and General injuries
18. (5) Which is the possible combination of General and local lesions in the disease?
general exclusive
3. all diseases first begins with local lesions, and subsequently appear and General injuries
5. some diseases begin with General injuries and later appear and local lesions
19. (3.5) that are variations of the combination of General and local lesions in the disease?
general exclusive
8. some diseases begin with local lesions, and subsequently appear and General injuries
10. some diseases begin with General injuries and later appear and local lesions
20. (2) What is the pathogenic factor?

1. the acting cause disease
2. all the phenomena which develops after the first action causes
3. the effect caused directly by the action of the first cause
4. the cause of the disease that has caused
5. conditions that cause of action favored disease
21. What is the chain of causes-effects in the pathogenesis of the disease?

1. the totality of cause-effect links from the beginning and up to rezoluţa disease
2. the totality of injuries encountered during the course of the disease
3. all of the body's reactions encountered over the course of the disease
4. all of the body's reactions and injuries encountered during the course of the disease
5. all of the body's reactions and injuries linked by cause and effect relationships
(5)
22. What is the main link to the pathogenesis?

1. the cause that has caused illness and removing that disappears and disease
2. acţina the first injuries causes and removing which disappears and disease
3. the last factor to eradicate the pathogenesis which disappears and disease
4. pathogenetic factor that depends on the development of the disease and the removal of
which disappears and disease
5. the first pathogenic factor at which disappears and disease eradication
(4)
23. (1) what is etiotropă therapy of the disease?

1. the therapy targeted at the removal of the cause of disease
2. the therapy targeted at removing the primary lesions
3. the therapy targeted at alleviating the pathogenic action of etiological factor
4. the therapy targeted at removing the main personnel Portal
5. the therapy targeted at overcoming the vicious circle
24. (4) what is disease pathogenetic therapy?

1. the therapy targeted at the removal of the body to cause disease
2. the therapy targeted at removing the primary lesions
5. the therapy targeted at removing all factors patogenetici
25. What is symptomatic therapy of the disease?

1. the therapy targeted at removing the primary lesions manifested clinically
4. the therapy targeted at overcoming the vicious circle
5. the therapy targeted at removing the patient's life threatening disorders
(5)
26. (1) presenting specific prophylaxis of the disease?

1. prevention through active or passive immunization
2. prevention through consumption of vitamins, trace elements
3. prevention through "tempering" the body
4. prevention through the creation of conditions for the person favoraabile
5. effective prophylaxis for a single patient
27. (2) what is the non-specific disease prophylaxis?

1. active or passive immunization
2. the consumption of vitamins, trace elements
3. prophylactic administration of antibiotics
5. avoiding contact with infected people
28. (2) what is the non-specific disease prophylaxis?
2. "tempering" the body
3. prophylactic administration of antibiotics
29. (2,3) representing non-specific disease prophylaxis

2. the healthy activity and rest
3. the consumption of vitamins, trace elements
30. (1) what is the physiological reaction of body feature?

1. corresponds to the excitantului specifics
2. it is effective only for an exciting
3. lead to persistent dishomeostazii
4. lower intensity is excitantului
5. d epăşeşte excitantului force
1. quantitative intensity corresponds to excitantului
5. exceeds the intensity of excitantului

1. homeostatic nature
6. it is effective for several exitanţi
34. (2.5) Which is characteristic of the physiological reaction of the organism?
11. it is effective for several exitanţi
15. homeostatic nature
35. (1.5) That is characteristic of the physiological reaction of the organism?

16. corresponds to the excitantului specifics
20. quantitative intensity corresponds to excitantului
36. (1) the characteristic pathological reaction of the organism?

2. lead to restoring the body's homeostasis.
3. is specific only for an exciting
4. corresponds to the intensitrăţii excitantului
5. meets and in physiological processes
1. exceeds the force excitantului

1. leads to dishomeostazii
39. (1.5) That is characteristic of pathological reaction of the organism?
40. (1.4) That is characteristic of pathological reaction of the organism?

14. exceeds the force excitantului
41. What is adaptive reaction?

1. the reaction focused on the change of function and structure of the organism in accordance
with the new conditions of existence
2. the reaction to the removal of harmful element in the body
3. the reaction focused on maintaining the tool body hiperfuncţia other infringed by sinergist
organ
4. the reaction focused on recovering the defect structure and structural restoration of
homeostasis
5. oriented modification phenotype reactions according to the conditions of existence
(1)
42. These compensatory reaction?

organ
homeostasis
(3)
43. What is the reaction of protective?

2. the reaction focused on mitigating action harmful to the body element
organ
homeostasis
(2)
44. What is the reaction of reparative regulation?

organ
homeostasis
(4)
45. (1) Which is the first period of the disease?

1. latent
2. prodromală
3. complete development of the disease
4. resolution
5. cardiac symptoms exacerbation
46. (2) it is the second time the disease?
1. latent
2. prodromală
4. resolution
47. (3) Which is the third period of the disease?
1. latent
2. prodromală
4. resolution
48. (4) is the fourth period of the disease?
1. latent
2. prodromală
4. resolution
49. What is the latent period of the disease?

1. the absence of any clinical manifestations
2. the lack of specific clinical manifestations
3. the presence of nonspecific clinical manifestations
4. the presence of specific and nonspecific events
5. the temporary disappearance of manifestations of disease
(1)
50. (3) what is the prodromală of the disease?
1. the absence of any symptoms
2. the presence of local events
3. nonspecific events prezenza
5. the temporary disappearance of manifestations of disease
51. What is full during the disease?

1. the absence of any symptoms
2. the lack of specific clinical manifestations
3. nonspecific events prezenza
5. the disappearance of manifestations of disease
(4)
52. (3) what is the resolution of the disease?

1. temporary disparţia of all manifestations of disease
2. the disappearance of specific events
3. monitor the death occurs
4. the disappearance of nonspecific events.
5. improvement of patient's condition
3. complete healing occurs
3. incomplete healing occurs
55. (3.5) what is the resolution of the disease?

10. monitor the death occurs
56. (3.5) what is the resolution of the disease?
15. complete healing occurs
57. What is the pathological process?

1. all of the primary lesions caused by the action of the first cause
2. all of the primary and secondary lesions caused by the action of the first cause
3. all primary and secondary injuries plus the physiological reactions of the organism
4. tortalitatea of local and General lesions caused by the action of the first cause
5. tortalitatea of the body's physiological reactions triggered by the action of the first cause
(3)
58. What are primary mechanisms sanogenetic?

1. Adaptive reactions, protective and compensatory
2. protective reactions, and terminals
3. Adaptive compensatory reactions and terminals
4. initial and Terminal mechanisms
5. adaptive, protective and compensatory reactions and terminals
(1)
59. the mechanisms of secondary sanogenetic?
2. protective reactions, and terminals
4. initial and Terminal mechanisms
5. adaptive, protective and compensatory reactions and terminals
(2)
60. What is the cercului vicious in pathogenesis?

1. totalitateof of causes and effects that make up the chainthe pathogenesis
2. itclosed anţ causes and effects in that last question causes the effect similar to the effect of
the first cause
3. the totality of pathological processes in which the last process has the same consequences
as the first trial
4. all related injuries through relationships of cause and effect
5. all physiological reactions linked by cause and effect relationships
(2)
1. itclosed anţ causes and effects which persist and after curing
2. itclosed anţ causes and effects that are automenţine and progressively deepening
3. itclosed anţ pathological processes within a illnesses related to causal relationships through
which autoamplifică
4. itclosed anţ related injuries through relationships of cause and effect which is
autoamplifică
5. itclosed anţ physiological reactions linked through relationships of cause and effect which
is autoamplifică
(2)
6. itclosed anţ causes and effects in that last question causes the effect similar to the effect of
the first cause
7. itclosed anţ causes and effects that are automenţine and progressively deepening
8. itclosed anţ pathological processes within a illnesses related to causal relationships through
which autoamplifică
9. itclosed anţ related injuries through relationships of cause and effect which is
autoamplifică
10. itclosed anţ physiological reactions linked through relationships of cause and effect which
is autoamplifică
(1,2)
2. CELLULAR DAMAGE (167)

1. What is theprimary cell insertion points into?
1. Any Injuries arising from the direct action of the organelles of the harmful factor
2. Lizozomilor Injuries as result of hypoxic acidosis
3. Mitochondria as consequence of Lesions increasing the concentration of K in hialoplasmă
4. Endoplasmic reticulum Injuries as a consequence of lipid peroxidation thus interrupting
5. Cytoplasmic membrane Lesions caused by the direct action of harmful element
(a)
2. what is thesecondary insertion points into the cell?

1. Any Injuries arising from the direct action of the organelles of the harmful factor
2. Any Injuries incurred as a consequence of the organelles lesion cytoplasmic membrane
3. The lesions caused by the direct action of the mitochondria of the harmful factor
4. Endoplasmic reticulum Injuries arising from the direct action of harmful element
5. Cytoplasmic membrane Lesions caused by the direct action of harmful element
(b)
3. How is cellular nonspecific lesions?

Cytoplasmic membrane permeability increase
Increased activity in the blood ALAT
Decreased activity of ALAT in blood
Increased activity of AST in the blood
Increased concentration of amylase in blood
(a)
4. (2) how to modidfică enzyme spectrum in lobular inflammation, injury of blood?
1. Increased activity of amylase in blood

2. Increased activity of AST in the blood
3. Increased activity of citocromoxidazei in the blood
4. Increased activity of trypsin in the blood
5. Increased activity of alkaline phosphatase in the blood
5. (1) how to modidfică enzyme spectrum in pancreas lesions of blood?

4. Increased activity in the blood AlAT
6. (4) how to modidfică enzyme spectrum in lesions of blood miocardiocitului ?

2. Increased activity of trypsin in the blood
7. (5) how to modidfică enzyme spectrum in epithelium lesions of blood bile ducts ?
8. What is the effect of mechanical lesion of the cytoplasmic membrane?

1. Load balancing intra-and extracellular concentrations of ions
2. intracellular Na scădereconcentraţiei
3. increasing the intracellular concentration of K
4. decreased concentration As in hialoplasmă
5. increased concentration of Ca in reticulum reticulum
(a)
6. Dizechilibrul intra-and extracellular concentrations of ions
7. increasing the intracellular concentration of Na
(b)
12. decreased concentration of intracellular K
(b)
17. decreased concentration of intracellular Na
20. increased concentration of Ca in hiloplasmă
(e)
12. What are the effects of cytoplasmic membrane mechanical lesion?
22. increased concentration of Ca in hiloplasmă
25. increased concentration of Ca in hialoplasmă
(c, e)
13. What are the effects of cytoplasmic membrane mechanical lesion?
30. increased concentration of Ca in hialoplasmă
(b, e)
14. What are the mechanical effects of cytoplasmic membrane?
(b, c)
15. What is the effect of electric current on the excitable cells?

1. Depolarizarea the cell membrane
2. Hiperpolarizarea the cell membrane
3. Repolarizarea cell membranes
4. Inhibition of electric pulse propagation
5. Contractibilităţii Mitigation miocitului
(a)
16. What is the effect of electric current on the excitable cells?
1. Hiperpolarizarea the cell membrane
2. Cell Excitation
(b)
17. What are the effects of electric current on the excitable cells?
6. Depolarizarea the cell membrane
1. Cell Excitation
(a, b)
18. What is the effect of the action of electric current of the cell?
1. Cytoplasmic membrane Hiperpolarzarea
2. Electrolysis of intracellular substances
3. The formation of excess NaCl
4. Cytoplasmic membrane Polarization
5. disassociation of intracellular substances
(b)
19. (1) The endogenous enzyme can cause damage of the cytoplasmic membrane?
1. Lysosomal Enzymes
2. Superoxid Dismutase
3. citocromoxidaza
4. dehidrogenazele
5. pancreatic amylase
1. The enzymes in inflammatory foci fagacitare cells
3. citocromoxidaza
4. dehidrogenazele
1. pancreatic trypsin
3. citocromoxidaza
4. dehidrogenazele
22. (1.2) that can cause damage to endogenous enzymes of cytoplasmic membrane?
7. Lysosomal Enzymes
8. citocromoxidaza
9. dehidrogenazele
23. (1.4) that can cause damage to endogenous enzymes of cytoplasmic membrane?
13. citocromoxidaza
14. The enzymes in inflammatory foci fagacitare cells
26. (1) what is the effect of high temperature direct action on the cell?
1. protein denaturation enzyme function
2. modification of membrane phospholipids
3. speed up biochemical reactions
4. distortion of ATP
5. cell dehydration
27. (1) what is the effect of low temperature direct action on the cell?
1. Crystallization of water and mechanical injury of cell membrane
2. protein denaturation enzyme function
3. distortion of the lesion and cell membrane phospholipids
4. formation of secondary autoalergene
5. cell dehydration
28. (1) what causes cell damage the extracellular dishomeostazie?
1. hyponatriemia associated
2. hipocalciemia
3. Hipokaliemia
4. hipomagneziemia
5. hipermagneziemia
29. (5) What causes cell damage the extracellular dishomeostazie?
1. hipocalciemia
2. Hipokaliemia
3. hipomagneziemia
4. hipermagneziemia
5. hipernatriemia
30. (4.5) What causes cell damage the extracellular dishomeostazii?
6. hipocalciemia
7. Hipokaliemia
8. hipomagneziemia
9. hyponatriemia associated
10. hipernatriemia
52. (2) what is the ratio of the concentration of ions in intracellular and extracellular K?
1. 1: 5
2. 4: 1
3. 1: 20 pm
4. 1: 10000
5. 100: 1
53. (1) the effect of which is to balance the concentration of intra-and extracellular
potassium?
1. Rest potential Annihilation
2. cytoplasmic membrane hiperpolarizarea
3. Hypokalemia
4. Hipernatriemie
5. Intracellular Dehydration
54. (3) what is the effect of increasing the concentration of potassium ions in extracellular
sector?
1. hiperosmolaritatea interstitial fluid
2. acidification of the interstitial fluid
3. depolarizarea adjacent cells
4. hiperpolarizarea adjacent cells
5. inflammation
55. (2) what is the ratio of the concentration of normal intra-and extracellular sodium?
1. 1: 5
2. 1: 20 pm
3. 4: 1
4. 1: 100
5. 1: 10000
56. (1) The process can cause decreased electrical resistance of the cytoplasmic membrane?
1. Splitting of membrane phospholipids
2. cytoplasmic membrane depolarizarea
4. cessation of activity of membrane pumps
5. opening of sodium channels
57. (1) what is the normal ratio of the concentration of calcium ions from the extracellular
space and hialoplasmă?
1. 1: 10000
2. 4: 1
3. 1: 100
4. 1: 5
5. 1: 20 pm
58. (1) what is the normal ratio of the concentration of calcium ions and hialoplasmă
reticulum in reticulum?
6. 1: 10000
7. 4: 1
8. 1: 100
9. 1: 5
10. 1: 20 pm
59. (1) the intracellular enzymes That enable to increase the concentration of Ca2 + in
hialoplasmă?
1. endonucleazele
2. the Krebs Cycle enzmele
3. glicolitice enzymes
4. lipolytic enzymes
5. Glicogensintetaza
hialoplasmă?
1. ATP-azele
hialoplasmă?
1. Fosfolipazele
hialoplasmă?
1. Proteases
63. (1.3) of intracellular enzymes enable the increased concentration of Ca2 + in
hialoplasmă?
6. Proteases
8. endonucleazele
64. (1.4) of intracellular enzymes That enable to increase the concentration of Ca2 + in
hialoplasmă?
11. Proteases
14. ATP-azele
65. (1.5) of intracellular enzymes enable the increased concentration of Ca2 + in
hialoplasmă?
16. Proteases
1. Fosfolipazele
66. (1) what is the effect of nonspecific activation of intracellular ATP azelor?
1. while ineffective ATP reserves
2. the use of ATP for intracellular processes
3. ATP regeneration stimulation
4. decreased levels of ADP
5. enhancement of oxidative fosforilării
67. (3) what is the effect of nonspecific activation of cellular endonucleazelor?

1. initiation of necrosis and cellular
2. initiating cell dystrophy
3. initiation of apoptosis of the cell
4. initiate cell autolizei
5. initiation sclerozării
68. (5) what is the effect of nonspecific activation of cellular fosfolipazelor?

1. activation of prostagalndinelor synthesis
2. activation of leucotrienelor synthesis
3. activation of kininelor synthesis
4. acumulaea in excess of arachidonic acid
5. cytoplasmic membrane destabilisation
69. (4) what is the effect of nonspecific activation of cellular proteazelor?

1. initiation of necrosis and cellular
2. initiating cell dystrophy
3. initiation of apoptosis of the cell
4. initiate cell autolizei
5. initiation sclerozării
70. (2) what is the cause of cellular acidosis?

1. activation of the Krebs cycle
1.depletion of intracellular buffer systems
2.activation of oxidative processes
3.reduced excretion of hydrogen ions with urine
4.excessive ingestion of acid substances
1. activating anaerobic catabolism

2. activation of oxidative processes
1.inhibition of Glycolysis
1. increased intracellular ion Influx of H

2.Glycolysis Inhibition
3.activation of oxidative processes
73. (3) Which is causing cellular acidosis?
1. cellular exacerbation "

3.cell hypoxia
5. reduced excretion of hydrogen ions with urine
74. (3,4) what causes cell acidosis?

5.cellular hypoxia
4.1. activating anaerobic catabolism
75. (2,3) Which causes cellular acidosis?

6. Depletion of intracellular buffer systems
7.cellular hypoxia
76. (3.5) That causes cellular acidosis?

9.cell hypoxia
5. increased intracellular ion Influx of H
77. (2) Which is the consequence of cellular decompensation of acidosis?

2. the Krebs Cycle enzyme inactivation
3. Permeabilitaţii Decrease of the cell membrane to ions of Na
5. activation of enzymes glicolitice

2.permeabilitaţii growth of the cell membrane to ions of Na
5. activation of enzymes glicolitice

2.activation of the enzymes glicolitice
3.glicolitice enzyme inactivation
5. reduction of the permeabilitaţii cell membrane for ions of Na

2.activation of the enzymes glicolitice
4.Activate and exit in Lysosomal enzymes hialoplasmă
5.reduction of the permeabilitaţii cell membrane for ions of Na
81. (1,4) what are the consequences of cell decompensation of acidosis?
6. 1. the Krebs Cycle enzyme inactivation

3.Activate the enzymes glicolitice
6.activation and output in Lysosomal enzymes hialoplasmă
7.permeabilitaţii reduction of cell membrane for ions of Na
4. permeabilitaţii growth of the cell membrane to Na + ions

5.activating enzymes glicolitice
8.Turn and exit in Lysosomal enzymes hialoplasmă
9.permeabilitaţii reduction of cell membrane for ions of Na
10. 1. glicolitice enzyme inactivation

6.activation of enzymes glicolitice
11. Turn and exit in Lysosomal enzymes hialoplasmă
87. (1) The contributor may disconnect the processes of oxidation and phosphorylation in
mitochondria?
1. Thyroxine
2. Hemoglobin
3. Stercobilin
4. Urobilina
5. Together With
88. (1) what is the effect of oxidation processes and setting loose phosphorylation?
1. decreasing the efficiency of biological oxidation
2. increasing the efficiency of biological oxidation
3. oxygen consumption
4. decrease calorigenezei
5. diminishing the use of ATP for the cell
1. increased oxygen consumption
2. biological oxidation efficiency at
5. reduction of ATP by the cell utiliării
1. calorigenezei growth
4. Reduction of ATP synthesis
92. (1), (4) what are the effects of setting loose oxidation and phosphorylation?
6. decreasing the efficiency of biological oxidation
93. (1,4) Which are the effects of oxidation processes and setting loose phosphorylation?
1. increased oxygen consumption
94. (1,4) Which are the effects of oxidation processes and setting loose phosphorylation?
15. calorigenezei growth
95. (1) Which is the consequence of shortages in cell enegetice?
1. cessation of activity of ionic pumps
2. inactivation of enzymes inracelulare
3. compensatory activation of ion pumps
4. the closure of ion channels
5. enhancing the anabolic cell processes

1. Annihilation-extracellular ionic gradient
7. compensatory activation of ion pumps
8. the closure of ion channels
9. enhancing the anabolic cell processes
1. cytoplasmic membrane Depolarizarea
4. inhibition of celuleli hiperpolarizabtă
5. decreasing the excitability of the cell
1. to increase the concentration of ADP with activation of oxidative processes
2. decreased concentration of ATP which activates oxidative processes
3. increasing the concentration of inorganic phosphorus which activates oxidative proceseer
4. Crebs cycle block
5. anaerobic Glycolysis block
1. to increase The content of2 + in hialoplasmă
2. decreased concentration of Ca2 + in hialoplasmă
3. to increase the content of Ca2 + in reticulum reticulum
4. decreased concentration of Ca2 + in reticulum reticulum
5. to increase The content of2 + in the intercellular space
100. (1.2) what are the consequences of shortages in cell enegetice?
1. cessation of activity of ionic pumps

1. Annihilation-extracellular ionic gradient
1. cytoplasmic membrane Depolarizarea

1. to increase the concentration of ADP with activation of oxidative processes
105. (1) Which is the consequence of Lysosomal membrane destabilisation?

1. the hydrolysis of protein of hialoplasmă compounds
2. the release of ions As in hialoplasmă
3. the release of Na ions in hialoplasmă
4. the release of K ions in hialoplasmă
5. apoptosis
1. cell autolysis
5. apoptosis
1. the Lysosomal enzymes in hialoplasmă
5. apoptosis
108. (1.3) Which are the consequences of Lysosomal membrane destabilisation?
8. the hydrolysis of protein of hialoplasmă compounds
10. apoptosis
109. (1.3) Which are the consequences of Lysosomal membrane destabilisation?
13. cell autolysis
15. apoptosis
110. (1) Which is destabilising factor of Lysosomal membranes?
1. hypoxia
2. Glucocrticoizii
3. Vitamin E
4. Vitamin C
5. vitamin A

1. ionizing radiation
2. Glucocrticoizii
3. Vitamin E
4. Vitamin C
5. vitamin A
1. free radicals
2. Glucocrticoizii
3. Vitamin E
4. Vitamin C
5. vitamin A
113. (1,4) destabilizatori factors of Lysosomal membranes?
6. free radicals
7. Glucocrticoizii
8. Vitamin E
9. hypoxia
10. vitamin A
114. (1,4) destabilizatori factors of Lysosomal membranes?

11. free radicals
12. Glucocrticoizii
13. Vitamin E
14. ionizing radiation
15. vitamin A
115. (1) Which is the stabilizing Lysosomal membranes?

1. Glucocrticoizii
2. Vitamin A
3. Lactic acid
4. Pyruvic acid
5. Thyroxine
116. (1) stabilizing factor is Lysosomal membranes?
1. Vitamin E
2. Vitamin A
3. Lactic acid
4. Pyruvic acid
5. thyroxine
116. (1.3) are Lysosomal membrane stabilizer destabilizatori factors?
6. Vitamin E
7. Vitamin A
8. Glucocrticoizii
9. Pyruvic acid
10. thyroxine
148. (4) what process leads to the generation of free radicals?
1. apoptosis
2. cellular dystrophy
3. hipoptermia
4. Hypoxia
5. hyperemia of arterial
1. apoptosis
3. hipoptermia
4. Exacerbation "
1. apoptosis
3. hipoptermia
4. Inflammation
1. apoptosis
3. hipoptermia
4. ischemia
152. (2,4) what processes lead to the generation of free radicals?
6. apoptosis
7. Hypoxia
8. hipoptermia
9. ischemia
153. (3,4) what processes lead to the generation of free radicals?
11. apoptosis
12. hipoptermia
13. Exacerbation "
14. ischemia
154. (4.5) what processes lead to the generation of free radicals?
16. apoptosis
18. hipoptermia
19. ischemia
20. Inflammation
155. (1) The substance refers to free radicals?

1. Superoxidul oxygen
2. hydrogen ion
3. Ms. cations and K
4. phosphate anions
5. type of anion
1. Hydrogen peroxide
2. hydrogen ion
3. cations of Na and K
4. phosphate anions
5. carbonate ion of
1. the hydroxide anion

2. hydrogen ion
3. cations of Na and K
4. phosphate anions
5. carbonate ion of
158. (1.3) What substances refers to free radicals?

7. hydrogen ion
1. Superoxidul oxygen
8. phosphate anions
9. carbonate ion of
159. (1.3) What substances refers to free radicals?

11. hydrogen ion
12. Hydrogen peroxide
13. phosphate anions
14. carbonate ion of
160. (1) What substance is part of endogenous antioxidant system?

1. vitamin E
2. citocromoxidaza
1. the Krebs Cycle enzymes
2. phospholipase A2
3. prostaglandins
161. (1) The substance belongs to the endogenous antioxidant system?
1. Catalase
citocromoxidaza
5. phospholipase A2
6. prostaglandins
162. (1) The substance belongs to the endogenous antioxidant system?
superoxid dismutase
7. citocromoxidaza
9. phospholipase A2
10. prostaglandins
163. (1,4) What substances are part of the endogenous antioxidant system?
superoxid dismutase
11. citocromoxidaza
1. vitamin E
13. prostaglandins
164. (1.4) What substances are part of the endogenous antioxidant system?
superoxid dismutase
14. citocromoxidaza
1. Catalase
16. prostaglandins
165. (1) the effect of the action of free radicals?
1. Lipid peroxidation
2. Stabilizing Lysosomal membranes
3. The intensification of the processes of energogeneză
4. ceşterea oxygen consumption
5. enhancement of anaerobic Glycolysis
166. (1) what is the effect of the action of free radicals?
1. Peroxidara and altering DNA

3. The intensification of the processes of energogeneză
167. (1.3) Which is the effect of the action of free radicals?
6. Peroxidara and altering DNA

8. Lipid peroxidation
3. PATHOLOGICAL CELLULAR PROCESSES (124)

CELLULAR DYSTROPHIES
1. (1) what is the cause of cellular Dystrophies?
1. dismetabolisme gebeale
2. General acute hypoxies
3. General dewatering
4. General hiperhidratarea
5. hiperproteinemia

6. General chronic hypoxies
10. hiperproteinemia
2. avitaminozele
5. hiperproteinemia

2. chronic poisoning
3. genrală dewatering
11. 4. General hiperhidratarea

2.dehydration genrală
3.inaniţia
6. (1.3) what are the causes of cellular Dystrophies?
13. 1. General chronic hypoxies
3.inaniţia
7. (1, 3) what are the causes of cellular Dystrophies?
6. 1. avitaminozele
3.inaniţia
8. (1, 3) what are the causes of cellular Dystrophies?
3. 1. chronic poisoning
3.inaniţia
9. (1) The pathological process in intracellular causes muscular dystrophy?

1. inhibition of the Krebs Cycle
2. apoptosis
3. aseptic necrosis
4. hypertrophy
5. atrophy
1. intracellular accumulation of Ca
2. apoptosis
3. aseptic necrosis
4. hypertrophy
5. atrophy

1. the accumulation of intracellular fatty acid
6. apoptosis
7. aseptic necrosis
8. hypertrophy
9. atrophy

1. intracellular acidosis
10. apoptosis
11. aseptic necrosis
12. hypertrophy
13. atrophy

1. enzimopatii cellular
14. apoptosis
16. hypertrophy
17. atrophy
14. (1.5) The intracellular pathological processes causes muscular dystrophy?

18. apoptosis
20. hypertrophy
21. inhibition of the Krebs Cycle
15. (1.5) that causes muscular dystrophy intracellular pathological processes?
22. apoptosis
24. hypertrophy
25. intracellular accumulation of Ca
26. apoptosis
28. hypertrophy
1. the accumulation of intracellular fatty acid
29. apoptosis
31. hypertrophy
1. intracellular acidosis
25. What is a specific manifestation of the dystrophy?

1. intumescenţa mitochondria
2. reduce endoplasmic reticulum
3. distrucţia ribozomilor
4. cytoplasmic membrane lesions
5. excessive deposition of glycogen
(5)
5. excessive deposition of lipids
(5)
5. excessive protein deposits anomale
(5)
28. What are the specific manifestations of dystrophy?

6. 1. excessive deposition of glycogen
(1.5)

6. 1. excessive deposition of lipids
(1.5)
30. What is the cause of parenchymal dislipidozelor?

1. excessive consumption of dietary carbohydrates
2. excessive consumption of food proteins
3. hiperinsulinismul
4. hyperthyroidism
5. hyper corticismul
(1)
2. lipoproteinlipazei failure
4. hyperthyroidism
(2)
3. hipoinsulinismul
4. hyperthyroidism
(3)
33. Which is the cause of parenchymal dislipidozelor?
3. inaniţia
4. hyperthyroidism
l
(3)
1. persistent Hyperlipidemia
2. insulin hipersecreţia
3. the cell's inability to synthesize glycogen
4. the inability to turn the cell lipids in glycogen
5. the cell's inability to synthesize ketone body of lipid bodies
(1)

1. synthesis of lipids in the cell anomale
3. the cell's inability to synthesize glycogen
(1)
39. What are the causes of parenchymal dislipidozelor?
1.1. persistent Hyperlipidemia
1. excessive consumption of dietary carbohydrates
(1.3)
10. lipoproteinlipazei failure
(1.3
14. hipoinsulinismul
(1.3)
18. inaniţia
(1.3)
1. inability to synthesize lipoproteins
(1.3)
1. persistent Hyperlipidemia
(1.3)
1. the insufficiency of lipolytic enzymes intracellular
(1.3)
1. inability to synthesize Phospholipid cell
(1.3)
54. (5) Which is one of the possible consequences of the Dystrophies and cellular?
1. cellular dediferenţierea
2. cellular hypertrophy
3. hyperplasia
4. hypoplasia
5. apoptosis
55. (5) Which is one of the possible consequences of the Dystrophies and cellular?
3. hyperplasia
4. hypoplasia
5. aseptic necrosis
56. (5)That is one of the possible consequences of cellular Dystrophies?
3. hyperplasia
4. hypoplasia
5. inflammation
57. (5)That is one of the possible consequences of cellular Dystrophies?
3. hyperplasia
4. hypoplasia
5. sclerosis
58. (1.5)What are the possible consequences of cellular Dystrophies?
6. apoptosis
8. hyperplasia
9. hypoplasia
10. sclerosis
59. (1.5)Which suntconsecinţele Dystrophies of cell?
13. hyperplasia
14. hypoplasia
15. sclerosis
60. (1.5)What are the possible consequences of cellular Dystrophies?
16. inflammation
18. hyperplasia
19. hypoplasia
20. sclerosis
APOPTOSIS
61. (2) The cells undergo apoptosis?
1. normal aging cells
2. normal cells beyond functional needs
3. dead cells
4. cellele sclerozate
5. cells with Dystrophies
2. cells with the gene defects
3. dead cells

2. cells infected with viruses
3. dead cells

2. cancerizate cells
3. dead cells

7. body cells subjected to physiological involution
8. dead cells
66. (2,4) cells undergo apoptosis?
13. dead cells
14. normal cells beyond functional needs
67. (2,3) The cells undergo apoptosis?
18. cells with the gene defects
23. cells infected with viruses
28. cancerizate cells
88. What is apoptosis during initiation?

1. intercellular communication structures disruption
2. disintegration of the cytoplasmic membrane of the cell
3. disintegration of the mitochondria
4. cariorexia
5. carioliza
(1)
1. selected strain condensation
4. cariorexia
5. carioliza
(1)
90. Through what manifests itself during apoptosis initiation?
1. condensation nucleus
4. cariorexia
5. carioliza
(1)
8. cariorexia
(1.5)
11. cariorexia
1. selected strain condensation
(1.5)
93. what condition is needed for conducting of apoptosis?

1. maintenance of the integrity of the cell membrane
2. preservation of the integrity of the kernel
3. preservation of the integrity of the cytoskeleton
4. preservation of the integrity of chromosomes
5. maintenance of intercellular connections
(1)
94. what condition is needed for the final deployment of apoptosis?

1. keeping the tool mitochondria
2. keeping the core cellular functions
3. rough endoplasmic reticulum function preservation
4. Golgi apparatus function preservation
5. maintenance of intercellular connections
(1)
95. What is apoptosis in the average period?

1. formation of apoptoticci bodies
2. disintegration of the corpora of apoptotic
5. cariorexia
(1)
96. Who is the phenomenon of apoptosis?

1. phagocytosis of apoptotic corpora
2. celulelie undergo apoptosis phagocytosis
3. disintegration of the extracellular matrix of apoptotic suppression components of
biochemical
4. degradation biochemical components of corpora apoptosis by the liver
5. biochemical components of excretion of apoptosis by the kidneys
(1)
ASEPTIC NECROSIS
115. what is necrosis?
1. cell death in pathogen factors
2. cell death after death of the body
3. cell death while genetic potential
4. the death of the cell while the potential functional
5. the death of the cell in the process of involution of the Caterpillar
(1)
120. Which is the weakest link in the pathogenesis of necrosis from the cytoplasmic
membrane injury?
1. disturbance of the function of ion channels
2. disruption of mitochondria function
3. Ionic pumps malfunction function
4. concenraţiei balancing intra-and extracellular Ionic
5. disruption of the cell nucleus funţiei
(4)
121. Who is the weakest link in the pathogenesis of infectious lesions in the mitochondria?
1. the opening of ion channels
2. intracellular protein deficiency
3. ATP dficitul
4. excess intracellular sodium
5. intracellular potassium deficiency
(3)
80. What is the main link of the pathogenesis of necrosis from the action of free radicals?
1. disintegration of the cytoplasmic membrane
2. intracellular hiperosmolaritatea
3. gene mutations
4. distrucţia intercellular connections
5. inflammation
(1)
98. (1) Which is the consequence of infectious?
1. local inflammation, enzimemie, hyperkalaemia
2. lack of local inflammation of enzimemiei and hiperkaliemiei
3. local inflammation, without enzimemie, without hyperkalaemia
4. lack of local inflammation, with enzimemie, with hyperkalaemia
10. the generalized inflammation
99. That is the consequence of infectious?
1. inflammation
2. hipernatriemie
3. hypokalemia
4. hipercalciemie
5. elimination of cells with irreparable damage
(1)
100. Which is the consequence of infectious?
1. enzimemie
2. hipernatriemie
3. hypokalemia
4. hipercaşciemie
(1)
101. Which is the consequence of infectious?

1. hyperkalaemia
2. hipernatriemie
3. hypokalemia
4. hipercaşciemie
5. removal of infected cells, irreparable damage, with non-viable mutations
(1)
102. That is the consequence of infectious?

1. hipernatriemie
2.hypokalemia
3.hipercaşciemie
4.development of inflammatory mediators
5.elimination of cells with irreparable damage
(4)
103. What are the consequences of infectious?

6. 1. inflammation
6.hypokalemia
7.hipercaşciemie
1.1. enzimemie
8.the Elimination of cells with irreparable damage
(1.4)

1.1. enzimemie
9.hypokalemia
10. hipercaşciemie
11. production of inflammatory mediators
(1.4)

1.1. Hyperkalaemia
13. hypokalemia
14. hipercaşciemie
15. production of inflammatory mediators
(1.4)

1.1. Hyperkalaemia
17. hypokalemia
18. hipercaşciemie
1.1. enzimemie
(1.4)
122. That is one of the consequences of infectious?

1. the fever
2. leucocitopenia
3. bacteriemia
4. hipernatriemia
5. hipecalciemia
(1)
123. it is one of the consequences of infectious?
1. acute phase reaction
2. leucocitopenia
3. bacteriemia
4. hipernatriemia
5. hipecalciemia
(1)
1. acute phase reaction
1. the fever
6. bacteriemia
7. hipernatriemia
8. hipecalciemia
(1,2)
4. PATHOLOGICAL TISSUE PROCESSES (77)
REGENERATION
1. what process is regenerative at the molecular level?

1. cytoplasmic membrane Phospholipid resinteza
2. resinteza DNA in neuron
3. DNA resinteza in miocardiocit
4. resinteza DNA in erythrocyte
5. the erythrocyte hemoglobin resinteza
(1)
1. the cytoskeleton protein resinteza
3. DNA resinteza in miocardiocit
(1)
1. resinteza Lysosomal enzymes
3. resinteza DNA in myocardium
(1)
1. resinteza actinei and miozinei in miocardiocit
2.resinteza DNA in neuron
3.resinteza DNA in myocardium
(1)
5. what regenerative processes at the molecular level are possible?
1. cytoplasmic membrane Phospholipid resinteza
(1.3)
1. resinteza Lysosomal enzymes
(1.3)
1. the cytoskeleton protein resinteza
(1.3)
8. what process is possible in regenerative organitelor cell?
1. multiplying the mitochondria
2.the multiplication of the nucleus
3.multiplication lizozomilor
4.ripping ribozomilor
5.the multiplication of cytoplasmic vacuolelor
(1)
1. the formation of new ribozomilor
2. multiplication of the nucleus
3. replication lizozomilor
4. replication ribozomilor
5. vacuolelor cytoplasmic multiplication
(1)

1.formation of lysozyme us
2.the multiplication of the nucleus
3.multiplication lizozomilor
4.ripping pibozomilor
5.the multiplication of cytoplasmic vacuolelor
(1)
6.formation of reticolului reticulum
7.multiplying the kernel
8.the multiplication of lizozomilor
9.pibozomilor multiplication
10. vacuolelor cytoplasmic multiplication
(1)
12. what regenerative processes are possible at the level of cellular organitelor?
11. formation of reticolului reticulum
14. replication pibozomilor
1. multiplying the mitochondria
(1.5)
19. the formation of new ribozomilor
(1.5)
24. formation of lysozyme us
(1.5)
15. What is pathological regeneration?

1. hip dysplasia
2. anaplazia
3. hypoplasia
4. Aplasia of
5. hyperplasia
(1)
1. metaplasia
2. anaplazia
3. hypoplasia
4. Aplasia of
5. hyperplasia
(1)
1. scar tissue
2. anaplazia
3. hypoplasia
4. Aplasia of
5. hyperplasia
(1)
1. tumour growth
2. anaplazia
3. hypoplasia
4. Aplasia of
5. hyperplasia
(1)
6. tumour growth
7. anaplazia
8. hypoplasia
9. hip dysplasia
10. hyperplasia
(1.4)

11. tumour growth
12. anaplazia
13. hypoplasia
14. metaplasia
15. hyperplasia
(1.4)

16. tumour growth
17. anaplazia
18. hypoplasia
19. scar tissue
20. hyperplasia
(1.4)
22. Why is hyperplasia?

1. cell population growth and body mass
2. body mass increase by increasing the volume of each cell
3. body mass increase by increasing the intercellular matrix
4. increasing body mass through the multiplcarea connective tissue cells
5. increasing the mass of the body fat deposition
(1)
23. What is hypertrophy?

1. increased body mass through population growth parenchymal cells
2. body mass increase by increasing the mass of the intercellular matrix
3. increasing body mass through population growth of connective tissue cells
4. increasing body mass through population growth of adipocytes
5. body mass increase by increasing the mass of the body framework
(1)
1. body mass increase by increasing the volume of each cell parenchimataose
3. princreşterea body mass population growth of connective tissue
4. increasing body mass through population growth of adipocytes
(1)
6. body mass increase by increasing the volume of each cell parenchimataose
8. princreşterea body mass population growth of connective tissue
1. increased body mass through population growth parenchymal cells
(1.4)
ATROPHY
30. What is the organ atrophy?
1. the reduction in volume of organs by decreasing the mass of parenchyma
2. the reduction in volume of organs by decreasing body fat mass
3. the reduction in volume of organs by decreasing the weight of the connective tissue
4. the reduction in volume of organs by decreasing the mass framework
5. the reduction in volume of bodies by dehydration
(1)
31. What is physiologic atrophy?

1. organ atrophy to the diminishing of the tool
2. endocrine glands atrophy in the hiposecreţia pituitary tropinelor
3. hormone dependent organs atrophy in the peripheral nervous system failure
4. organ atrophy in hypoperfusion
5. the body denervation atrophy
(1)
1. organ atrophy during certain periods ontogenetic
2. peripheral endocrine glands atrophy in the hiposecreţia pituitary tropinelor
3. hormone dependent organs atrophy in the respective hormone insufficiency
4. organ atrophy through hiponutriţie
(1)
1. înbătrânirea body organs to atrophy
(1)
10. organ atrophy to the diminishing of the tool
(1.5)
15. organ atrophy during certain periods ontogenetic
(1.5)
36. What is pathological atrophy?

1. organ atrophy to the pathogenic factor
2. prostate gland atrophy in men senili
3. atrophy of the thymus with age
4. skeletal muscle atrophy in people in hipodinamie
5. bone atrophy at cosmonauts in weightlessness
(1)
1. organ atrophy in ischemia
(1)
1. organ atrophy at the action of machinery
(1)
1. organ atrophy in the absence of growth factors
(1)
10. organ atrophy in ischemia
(1.5)
15. organ atrophy to the pathogenic factor
(1.5)
20. organ atrophy at the action of machinery
(1.5)
SCAR TISSUE
43. What is scar tissue organ?

1. pathological regeneration
2. physiological reparative regeneration
3. physiological compensatory regeneration
4. physiological protective, regenerating
5. the last stage of inflammation
44. The factor causing scar tissue?

1. cellular injuries
2. sustarea cell mitosis
3. hipofuncţia of oragnului
4. the lack of growth factors
5. apoptosis
(1)
1. cellular Dystrophies
5. apoptosis
(1)
1. cellular necrosis
5. apoptosis
(1)
1. chronic inflammation
5. apoptosis
(1)
48. what factors cause scar tissue?
8. cellular injuries
10. apoptosis
(1.3)
13. cellular Dystrophies
15. apoptosis
(1.3)
18. cellular necrosis
20. apoptosis
(1.3)
51. What is pathogenesis of sclerozării?

1. the proliferation of connective tissue neogeneza fibroblaştilor
2. dediferenţierea fibroblaştilor and their abundant proliferation
3. the intense production of collagen by macrofagi
4. Elimination of intracellular Collagen fibers in the interstice
5. basic substance transformation in collagen
(1)
52. What is the pathogenesis of sclerozării?
1. abundant collagen synthesis without fibroblaştilor proliferation
(1)
1. increase the relative weight of the connective tissue due to reduction of parenchyma
(1)
1. chronic inflammation of the organ
(1)

4.1. the proliferation of connective tissue neogeneza fibroblaştilor
(1.4)
4.1. abundant collagen synthesis without fibroblaştilor proliferation
(1.4)
4.1. increase the relative weight of the connective tissue due to reduction of parenchyma
(1.4)
58. What is the mechanism to reduce the surplus of collagen in the body?
1. phagocytosis Collagen fibers with intracellular split
2. excess collagen excretion with urine
3. transformation of collagen fibers in elastic fibers
4. the transformation of fibrociţilor into parenchiamatoase cells
5. fibrociţilor apoptosis
(1)
59. What is the mechanism to reduce the surplus of collagen in the body?
1. the degradation of extracellular matrix by the action of enzymes colagenolitice
2. excess collagen excretion with urine
(1)
60. the mechanisms to reduce the surplus of collagen in the body?

(1,2)
61. what process leads to pathological progresantă sclerosis?

1. extended local hypoxia
3. hyperemia of arterial îndelingată
4. increased apoptosis of parenchymal organ
5. hipersecreţia of glucocorticosteroizi
(1)

1. alteraţia massive and the collapse of the parenchyma
(1)

(1)

1. limfodinamice local Haemostatic disorders
(1)

1. congenital defects of colagenolitice mechanism
(1)
66. The Pathologic processes leading to sclerosis progresantă?

8. extended local hypoxia
(1.3)

13. alteraţia massive and the collapse of the parenchyma
(1.3)

(1.3)

23. limfodinamice local Haemostatic disorders
(1.3)
70. What is the consequence of sclerozării?

1. body hipofuncţia
2. body malignizarea
3. body fat dystrophy
4. organ hypertrophy
5. dediferebnţierea
(1)
6. body deformation
(1)

11. body reshaping
(1)
73. What are the consequences of sclerozării?
16. body reshaping
(1.3)
74. What are the consequences of sclerozării?
21. body reshaping
(1.3)
75. What is the principle of the sclerozării pathogenetic correction?

1. stop the fibrilogenezei
2. inflamţiei local origination
3. surgical removal of the excess of connective tissue
4. inhibition of colagenolizei
5. stimulate the replication of parenchymal cells
(1)
76. Which is pathogenetic correction of sclerozării principiulul?
6. colagenolizei stimulation
7. inflamţiei local origination
(1)
77. What are the principles of the sclerozării pathogenetic correction?
11. colagenolizei stimulation
12. stop the fibrilogenezei
(1,2)
5. INFLAMMATION (177)
1. (1) In the inflammatory mediators from cells?
1. mast cells
2. parenchmatoase cells
3. red cells
4. ribbed miocite
5. neurons

6. monocytes
8. red cells
9. ribbed miocite
10. neurons
11. leukocytes granulocytes
13. red cells
14. ribbed miocite
15. neurons
16. fibroblasts
18. red cells
19. ribbed miocite
20. neurons
21. platelets
23. red cells
24. ribbed miocite
25. neurons
6. (1.5) of the inflammatory mediators from cells?
26. platelets
28. red cells
29. ribbed miocite
30. mast cells

31. platelets
33. red cells
34. ribbed miocite
35. monocytes

36. platelets
38. red cells
39. ribbed miocite
40. leukocytes granulocytes

41. platelets
43. red cells
44. ribbed miocite
45. fibroblasts
10. What is the effect of the mast in inflamţie triptazei?

1. Stimulate the complement alternative route
2. The drug activates complement classical way
3. Cleaves tryptamine
4. vasodilator
5. vasoconstrictor effect
(1)
11. What is the effect of the mast in inflamţie: triptazei
1. Contributes to the formation of C3-C9 fragments of complement
2. Contriubuie the formation of C3b fragments C3a and complement
3. Activates the complement fragmentu C1
4. Inhibits the complement C1q fragmentu
5. exhaust balance
(2)
12. What is the effect of the mast in inflamţie: triptazei
2. Contriubuie in the formation of the membrane attack complex
4. vasodilator
5. vasoconstrictor effect
(2)
13. What are the effects of mast in inflamţie: triptazei
9. vasodilator
10. Stimulate the complement alternative route
(2.5)
14. What are the effects of mast in inflamţie: triptazei
14. vasodilator
15. Contriubuie the formation of C3b fragments C3a and complement
(2.5)
15. what chimiotactic factor frees mast?

1. Chemotactic Factor of neutrophils
2. Chemotactic Factor of T lymphocytes
3. Chemotactic Factor of B lymphocytes
4. Chemotactic Factor of bazofilelor
5. The mast cell chemotactic Factor
(1)
1. The eosinophil chemotactic Factor
(1)
5. The monocytes chemotactic Factor
(5)
18. what factors chimiotactici release mast?

9. Chemotactic Factor of neutrophils
(4.5)
19. what factors chimiotactici release mast?

14. The eosinophil chemotactic Factor
(4.5)
20. What are the enzyme required for the synthesis of prostaglandins?
1. phospholipase A2 and cyclooxygenase
2. cyclooxygenase and lipooxigenaza
3. phospholipase A2 and lipooxigenaza
4. lecitinaza and cyclooxygenase
5. triptaza and cyclooxygenase
(1)
21. What is the enzyme required for the synthesis of leucotrienelor?

1. phospholipase A2 and cyclooxygenase
2. cyclooxygenase and lipooxigenaza
3. phospholipase A2 and lipooxigenaza
4. lecitinaza and cyclooxygenase
5. triptaza and cyclooxygenase
(3)
22. What is the effect of prostaglandin in inflammatory foci?

1. vasodilation
2. vasoconstriction
3. bronhoconstricţie
4. action uteroparalitică
5. hypertension
(1)
23. That the biological effect tromboxanilor reste in inflammatory foci?

1. stimulates aggregation plachetară
2. suppress the aggregation plachetară
3. action vasoconsrictoare
4. action bronhoconsrictoare
5. action uterotonică
(1)
24. What is the effect of prostacyclin in inflammatory foci?

4. action bronhoconsrictoare
5. action uterotonică
(2)
25. What is the effect of leukotriene in biological inflammatory foci?
1. vasodilating action
2. procoagulant effect
(1)
26. What general effect has Interleukin 1 (IL-1)?

1. action pirogenă
2. anti-inflammatory action
3. anabolic action
4. action chimiotactică
5. action eritropoietică
(1)
7. what effect exercise Interleukin 1 (IL-1) in inflammatory foci?

1. Activate the lymphocytes Th.
3. anabolic action
(1)
28. what effects exercise Interleukin 1 (IL-1) in inflammatory foci?
6. Activate the lymphocytes Th.
2. action pirogenă
(1.3)
29. What does the inflammatory mediator originates in neutrophil leukocytes?

1. Lysosomal enzymes
2. histamine
3. triptaza
4. histaminaza
5. anti-microbial antibodies
(1)
30. what inflammatory mediator originates in neutrophil leukocytes?
1.histamine
2. triptaza
3. histaminaza
4. reactive oxygen species
(4)
1. histamine
2. triptaza
3. histaminaza
4. halogenated compounds
(4)
1. histamine
2. triptaza
3. prostaglandin
4. cationic protein
(4)
33. what inflammatory mediators from neutrophil leukocytes?
6. 1. Lysosomal enzymes
2. triptaza
3. prostaglandin
4. cationic protein
(1.4)
34. what kind of inflammatory mediators from neutrophil leukocytes?

1.4. reactive oxygen species
2. triptaza
3. prostaglandin
4. cationic protein
(1.4)
35. what inflammatory mediators from neutrophil leukocytes?

1.4. halogenated compounds
2. triptaza
3. prostaglandin
4. cationic protein
(1.4)
36. what bacterici factor oxigendependent is generated by neutrophil leukocytes?

1. superoxide anion a-2
2. ozone O3
3. Br-
4. Ag
5. HCl
(1)
1. hydrogen peroxide H2O2
2. an ozone3
3. Br-
4. Ag
5. HCl
(1)
1. hydroxyl radical OH-
2. an ozone3
3. Br-
4. Ag
5. HCl
(1)
1. halogenatul OCl-
2. an ozone3
3. Br-
4. Ag
5. HCl
(1)
40. what factors bactericizi oxigendependenţi are generated by the neutrophil leukocytes?
1. halogenatul OCl-
2. an ozone3
3. Br-
4. Ag
5. a superoxide anion-2
(1.5)
1. halogenatul OCl-
2. an ozone3
3. Br-
4. Ag
5. hydrogen peroxide H2O2
(1.5)
1. halogenatul OCl-
2. an ozone3
3. Br-
4. Ag
5. OH hydroxyl radical-
(1.5)
43. What does bacteriostatic factor is generated by neutrophil leukocytes?
1. lactoferrin
2. antibacterial antibodies
3. activated complement
4. histaminaza
5. hyaluronidase
(1)
44. The mediator inflamartor comes from eosinophils?
1. cationic protein
2. histamine
3. antiparasitic antibodies
4. lysozyme
5. hyaluronidase
(1)
45. The mediator inflamartor comes from eosinophils?
1. histamine
2. perforina
4. lysozyme
5. hyaluronidase
(2)
46. what inflamartori mediators from eosinophils?
2. cationic protein
1. perforina
3. lysozyme
4. hyaluronidase
(1,2)
46. what inflammatory mediator originates from platelets?

1. serotonin
2. histamine
3. activator of platelet factor
4. chemotactic factor
5. tromboxanii
(1)
48. what inflammatory mediator originates in lymphocytes?
1. for lymphocyte mitogen factor
2. the activator of the complement factor
4. integrins
5. immunoglobulins
(1)
49. what inflammatory mediator originates in lymphocytes?
2. limfocitotoxina
4. integrins
5. immunoglobulins
(2)
50. The inflammatory mediator originates in lymphocytes?

2. chimiotactic factor for lymphocytes
4. integrins
5. immunoglobulins
(2)
51. The inflammatory mediator originates in lymphocytes?

3. inhibitory factor of migration mononuclearilor
4. integrins
5. immunoglobulins
(3)
52. The inflammatory mediators from lymphocytes?

9. for lymphocyte mitogen factor
10. immunoglobulins
(3,4)
53. what kind of inflammatory mediators from lymphocytes?
14. limfocitotoxina
15. immunoglobulins
(3,4)
54. The inflammatory mediators from lymphocytes?
19. chimiotactic factor for lymphocytes
20. immunoglobulins
(3,4)
55. what biologically active factor are initiated to complement activation?

1. C3
2. C5
3. C5-C9
4. C9
5. C1a
(3)
6. C3a
7. C3
8. C5
9. C9
10. C1a
(1)
11. C3
12. C5a
13. C5b
14. C9
15. C1a
(2)
58. what factors biologically active compounds are formed from complement activation?
16. C3
17. C5a
18. C5b
19. C5-C9
20. C1a
(2,4)
59. what factors biologically active compounds are formed from complement activation?
21. C3
22. C5a
23. C5b
24. C3a
25. C1a
(2,4)
60. What is the effect of C3a and C5a in inflammatory foci?

1. permeabilizarea blood vessels
2. action effects
3. stimulates the synthesis of prostaglandins
4. anticoagulant action
5. action procoagulantă
(1)
1. action effects
2. action as vasodilators
3. stimulates synthesis of prostaglandins
4. the anticoagulant action
5. procoagulantă action
(2)

1. action effects
2. stimulate the synthesis of prostaglandins
3. mast cells ' degranulation
4. the anticoagulant action
5. procoagulantă action
(3)
1. action effects
3. action chemotactică
4. anticoagulant action
(3)
64. What are the effects of C3a and C5a in inflammatory foci?
6. action effects
9. permeabilizarea blood vessels
(3,4)
11. action effects
2. action as vasodilators
(3,4)
15. action effects
3. mast cells ' degranulation
(3,4)
67. What is the effect of the contact factor Hageman enabled?

1. anticoagulant system
2. chemotactic effect
3. anti-inflammatory effect
4. direct distrucţia of the vascular wall
5. human Thrombin inactivation
(1)
2. activation of the fibrinolytic system
5. human Thrombin inactivation
(2)
3. activation kininogenetic
5. Human Thrombin inactivation
(3)
70. What are the effects of the contact factor Hageman enabled?
6. 5. activation anticoagulant
(3.5)
71. What are the effects of the contact factor Hageman enabled?
5. activation of the fibrinolytic system
(3.5)
72. What is the effect of kininelor in inflammation?

1. vasodilation
2. vasoconstriction
3. relax the uterine muscles
4. systemic hypertension
5. bactericide
(1)
1. vasoconstriction
2. contraction of smooth muscles of internal organs
5. bactericide
(2)
1. vasoconstriction
3. systemic hypotension
5. bactericide
(3)
1. vasoconstriction
2.relax the uterine muscles
3.systemic hypertension
4.the sensation of pain
5.bactericide
(4)
76. What are the effects of kininelor in inflammation?
1. vasoconstriction
6. vasodilation
7.systemic hypertension
8.the sensation of pain
9.bactericide
(2,4)

1. vasoconstriction
1. contraction of smooth muscles of internal organs
11. the sensation of pain
12. bactericide
(2,4)
1. vasoconstriction
1. systemic hypotension
14. the sensation of pain
15. bactericide
(2,4)
79. What is the sequence of reactions in vascular inflammatory foci?

1. ischemia-arterial-venous hyperemia hyperemia-stasis
2. ischemia-venous-arterial hyperemia hyperemia-stasis
3. stasis-ischemia-arterial-venous hyperemia hyperemia
4. ischemia-blood-stasis hyperemia-venous hyperemia
5. hyperemia of arterial-venous-stasis hyperemia-ischemia
(1)
80. what causes arterial inflammatory hyperemia mediator?
1. histamine
2. catecolaminele
3. interleukins
4. leucotrienele
5. complement factor C5-C9
(1)
catecolaminele
interleukins
leucotrienele
the coplementului C3a and C5a
complement factor C5-C9
(4)
1. catecolaminele
2. interleukins
3. leucotrienele
5. prostaglandins PGE2
(5)
1. catecolaminele
2. interleukins
3. leucotrienele
5. bradykinin
(5)
84. what causes inflammatory mediators hyperemia pressure?
6. histamine
7. interleukins
8. leucotrienele
10. bradykinin
(1.5)
the coplementului C3a and C5a
11. interleukins
12. leucotrienele
14. bradykinin
(1.5)
15. prostaglandins PGE2
16. interleukins
17. leucotrienele
19. bradykinin
(1.5)
87. That is a feature of the inflammatory pressure hiperemiei?

1. persistent character
2. transient character
3. neuroparalitică pathogenesis
4. pathogenesis neuroton
5. it is associated with reduction of permeability vacsulare
(1)
88. What is a feature of the inflammatory pressure hiperemiei?
1. mioparalitică pathogenesis
(2)
89. Which is a feature of the inflammatory pressure hiperemiei?
4. it is associated with increased permeability vacsulare
(4)
90. What are the features of arterial inflammatory hiperemiei?
2. persistent character
(1.4)
91. What are the features of arterial inflammatory hiperemiei?
3. mioparalitică pathogenesis
(1.4)
92. What is pathogenesis of vascular inflammation in hiperpermeabilizării?

1. the action of histamine
2. action tromboxanilopr
3. the action of prostacyclin
4. the action of hormones glucocortocosteroizi
5. the action of acetylcholine
(1)
4. the action of bradykinin
6. the action of acetylcholine
(3)
4. actvi factors of complement C3a and C5a
5. "central effects
(4)
10. the action of histamine
(4.5)
97. Who is hiperpermeabilizării in vascular pathogenesis of inflammation?

15. the action of serotonin
(4.5)

20. the action of bradykinin
(4.5)
99. What is venous hiperemiei inflammatory pathogenesis?

1. hemoconcentraţia in microvasele inflammatory Firebox
2. veins in inflammatory foci ablation
3. increase in the number of leukocytes into inflammatory Firebox capillaries
4. platelet aggregation in the sore organ
5. arterioles in inflammatory foci thrombosis
(1)
3. platelet aggregation under the action tromboxanilor
4. platelet aggregation under the action of prostacyclin
(3)
101. Who is hiperemiei venous inflammatory pathogenesis?
4. interstitial edema and increased pressure in the focus of inflammation
(4)
4. sferizarea endoteliocitelor
(4)
4. leukocyte in Capillary Wall
(4)
4. venulelor thrombosis in inflammatory foci
(4)
5. lymph in clotting of the lymph vessels inflammatory foci
(5)
7. hemoconcentraţia in microvasele inflammatory Firebox
(2.5)
12. platelet aggregation under the action tromboxanilor
(2.5)
17. interstitial edema and increased pressure in the focus of inflammation
(2.5)
109. Who is hiperemiei venous inflammatory pathogenesis?
22. sferizarea endoteliocitelor
(2.5)
27. leukocyte in Capillary Wall
(2.5)
32. venulelor thrombosis in inflammatory foci
(2.5)
112. What is the importance of biological hiperemiei and venous stazei inflammatory?
1. contributing to the emigration of leukocytes
2. the inflammatory process leads to children pyelonephratis
3. contribute to proliferation and regeneration in inflammatory foci parenchyma
4. infusion increases with blood sore tissue
5. contribute to the dissemination of the pathogen factor
(1)
2. contribute to exsudare
3. contribute to proliferation and regeneration of parenchymal inflammatory in the focus
4. increases blood infusion to the inflamed tissue
5. contribute to the dissemination of fectorului pathogen
(2)
2. contribute to the localization of inflammatory process
5. contribute to the dissemination of fectorului pathogen
(2)
10. contributing to the emigration of leukocytes
(2.5)
15. contribute to exsudare
(2.5)
117. it is in the focus of exsudaţiei inflammatory pathogenesis?

1. capillary hydrostatic pressure increases;
2. reduction of hydrostatic pressure the interstice
3. reduction of interstitial oncotice pressure;
4. reduction of pressure intracapilare; oncotice
5. the reduction of interstitial osmotic pressure
(1)
118. That is the focus of exsudaţiei inflammatory pathogenesis?
1. increased pressure oncotice interstitials;
2. reduction of hydrostatic pressure interstice;
(1)
119. That is the focus of exsudaţiei inflammatory pathogenesis?
1. hiperpermeabilizarea vascular wall;
(1)
120. Which is the focus of exsudaţiei inflammatory pathogenesis?
1. increased interstitial osmotic pressure;
(1)
121. What is exsudaţiei in the focus of the inflammatory pathogenesis?
2.1. capillary hydrostatic pressure increases;
(1,2)
122. Which is the focus of exsudaţiei inflammatory pathogenesis?
2.1. oncotice interstitial pressure rise;
(1,2)
123. What is exsudaţiei in the focus of the inflammatory pathogenesis?
2.1. hiperpermeabilizarea vascular wall;
(1,2)
124. That is the hallmark of serous exsudatului?

1. protein contains up to 2-3%
2.contains fibrin
3.contains many white polimirfonucleare
4.contains many erythrocytes
5.contains many platelets
(1)
125. That is the hallmark of exsudatului fibrinos?

21. contains fibrinogen
22. contains fibrin
23. contains Collagen fibers
24. contain elastic fibers
(3)
126. That is the hallmark of festering exsudatului?

1. contains fibrinogen
2. contains many white polimirfonucleare
3. contains many erythrocytes
4. contains many platelets
(3)
127. That is the hallmark of hemorrhagic exsudatului?

1. contains contains blood
2. contains fibrin
3. contains hemoglobin
4. contains many erythrocytes
5. contains many platelets
(4)
128. That is the mechanism of emigration of leukocytes into inflammatory foci?
1. chemotactici factors of inflammatory foci
2. filtraţia of leukocytes through outward processing in the vascular wall
3. electrokinetică in the electric displacement
4. the action forces Van derVaals
5. centifugi forces in blood torrent
(1)
129. What is the mechanism of emigration of leukocytes into inflammatory foci?
1. hiperpermeabilitatea vessels
4. the action forces Van der Weert
(1)
1. leukocyte of vacsular wall
(1)
2. the action of enzymes hidrolitice on the basement membrane of the vascular wall
(2)
132. Which is the mechanism of emigration of leukocytes into inflammatory foci?
2. selectinelor and expression of integrins on the cytoplasmic membranein the
endoteliocitelor and leukocyte
(2)
133. the mechanisms of emigration of leukocytes into inflammatory foci?
2. chemotactici factors of inflammatory foci
(2.5)
1. hiperpermeabilitatea vessels
(2.5)
9. leukocyte of vacsular wall
(2.5)
14. the action of enzymes hidrolitice on the basement membrane of the vascular wall
(2.5)
137. the biological impoprtanţa of Leukocyte neutrophil emigration in inflammatory foci?

1. cationic proteins, perforinei release
2. the release of free radicals, halogenaţilor
3. local specific immunity (antibody synthesis)
4. phagocytosis of dead cells and cellular detritului
5. capture and degradation of histamine
(2)
138. the biological impoprtanţa of Leukocyte neutrophil emigration in inflammatory foci?
2. phagocytosis of microorganisms
(2)
139. That is biological impoprtanţa leukocyte neutrophil emigration in inflammatory foci?
(2,4)
140. What is biological impoprtanţa leukocyte emigration eosinophils in inflammatory

foci?
(1)
foci?
(5)
foci?
(2.5)
143. What is biological impoprtanţa in the focus of inflammatory monocytes emigration?

1. generation of bactericidal substances (cationic protein, perforine)
2. collagen synthesis
(5)
144. the lymphocyte emigration biological impoprtanţa in inflammatory foci?
2. generation of bactericideoxigendependente substances (free radicals, halide)
3. local specific immunity (antibody synthesis, cellular immune reaction)
(3)
145. What is biological impoprtanţa lymphocyte emigration in inflammatory foci?
8. granulomului formation
(3)
146. the lymphocyte emigration biological impoprtanţa in inflammatory foci?
13. granulomului formation
15. local specific immunity (antibody synthesis, cellular immune reaction)
(3.5)
153. What is the source of proliferation in cell inflammatory foci?

1. parenchimale cells
2. the cells formed in the result metaplaziei
3. mutant cells
4. hematopoietic stem cells-blood German rock band
5. the cells formed in the result dediferenţierii
(4)
3. mutant cells
4. the German rock band blood monocyte
(4)
3. mutant cells
(4)
156. That is the source of proliferation in cell inflammatory foci?
1. parenchimale-resident cells
3. mutant cells
4. mesenchymal cells-resident
5. the cells formed in the result anaplaziei
(4)
157. Which are the sources of proliferation in the focus of cellular inflammatory?
8. hematopoietic stem cells-blood German rock band
(3,4)
158. What are sources for cellular proliferation in inflammatory foci?
(3,4)
159. Which are the sources of proliferation in the focus of cellular inflammatory?
(3, 4)
160. the biological significance of proliferation in inflammatory foci?

1. restoring the altered structures parenchimale
2. restoring the altered mesenchymal structures
3. boost angiogenezei
4. increase in abundance of parenchimale structures with the formation of protective barrier
5. the formation of excessive population of mesenchymal cells with ecological and protective
function
(5)
161. what process includes physiological regeneration in inflammatory foci?

1. restore specific structures parenchimale
2. training in excess of specific structures parenchimale
3. excess formation unspecific mesenchymal structures
4. de novo angiogenesis
5. the formation of collagen fibrils in excess
(1)
2. restoration of nonspecific mesenchymal structures
(2)
3. restoration of blood vessels
(3)
3. restoring the intercellular matrix
(3)
165. what processes include physiological regeneration in inflammatory foci?
6. restore specific structures parenchimale
(1.3)
166. what processes include physiological regeneration in inflammatory foci?
11. restoration of nonspecific mesenchymal structures
(1.3)
167c. what processes include physiological regeneration in inflammatory foci?
(1.3)
170. That is one of the manifestations of the body in General inflammatory reaction?
1. fever
2. hypothermia
3. leucocitopenia
4. allergic reactions
5. increased anabolism
(1)
171. That is one of the manifestations of the body in General inflammatory reaction?
1. hypothermia
2. Leukocytosis
3. leucocitopenia
4. the immunodeficiency
(2)
172. That is one of the manifestations of inflammatory reaction in the body?

1. hypothermia
2. leucocitopenia
3. slowing the VSH
4. speeding up the VSH
(4)
173. What is one of the manifestations of the body in General inflammatory reaction?
1. hypothermia
2. leucocitopenia
4. increased catabolism
(4)
174. which are the manifestations of the body in General inflammatory reaction?
2. fever
1. leucocitopenia
(1.4)
175. General manifestations of which are the body's inflammatory reaction?

5. Leukocytosis
6. leucocitopenia
(1.4)
176. What are the General manifestations of inflammatory reaction in the body?
10. speeding up the VSH
11. leucocitopenia
(1.4)
177. what hormone possess direct anti-inflammatory?

1. ACTH
2. Cortisol
3. aldosterone
4. Thyroxine
5. Testosterone
(2)
6. fever.STRESS (114)
1. what factors exogenous infectious pirogeni?
1. bacterial antigens
2. allogeneic transplantation
3. hyperimmune sera
4. blood and blood plasma heterogeneous
5. heterogeneous proteins parenteraal administered
(1)
1. bacterial endo-and exotoxine
3. hyperimmune sera
(1)
1. microbial lipopolizaharidele
3. hyperimmune sera
(1)
1. microbial, viral proteins, fungal
3. hyperimmune sera
(1)

8. hyperimmune sera
(1,2)
12. bacterial antigens
13. hyperimmune sera
(1,2)
17. bacterial endo-and exotoxine
18. hyperimmune sera
(1,2)
8. what factors exogenous neinfecţioşi pirogeni?

1. heterogeneous administered parenteral protein
2. isotonic solution of sodium chloride
3. isotonic glucose solution
4. hypertonic solution of glucose
5. Ringer solution
(1)
9. what factors exogenous neinfecţioşi pirogeni?

3. hypertonic solution of sodium chloride
5. Ringer solution
(3)
10 pirogeni exogenous factors neinfecţioşi?

8. hypertonic solution of sodium chloride
10. Ringer solution
(1.3)
11. What are the primary endogenous pirogenii ?

1. own cell disintegration products
2. insulin
3. immunoglobulins
4. glucocorticosteroizii
5. ACTH
(1)
1. hemolizei of own products
2. insulin
3. immunoglobulins
5. ACTH
(1)
1. hormones progestageni
2. insulin
3. immunoglobulins
5. ACTH
(1)
8. immunoglobulins
10. ACTH
(1,2
13. immunoglobulins
15. ACTH
(1,2
16. pirogeni endogenous factors are secondary?

1. cellular necrosis ischemic products
5. IL-1
(5)
5. IL-2
(5)
5. interleukin IL-6
(5)
5. TNF-alpha
(5)

6. IL-1
10. TNF-alpha
(1.
11. IL-2
15. TNF-alpha
(1.5)
16. interleukin IL-6
20. TNF-alpha
(1.5)
23. What is the relationship between termogeneză and termoliză during the foot?
1. Concomitant Stimulation of termogenezei and termolizei
2. Termogenezei Stimulation and inhibition of termolizei
3. The inhibition and activation of termolizei termogenezei
4. Inhibition of termogenezei and concomitant termolizei
5. Discordanţa activity of termogeneză and termoliză
(2)
24. What is one of the mechanisms of activation of termogenezei in fever?

1. Excitation of the sympathetic autonomic nervous system
2. Excitation parasympathicus portion of the autonomic nervous system
3. Hipersecreţia anaboizanţi hormones
4. Turn on lipogenezei and glicogenogenezei
5. Tonic Contraction of skeletal muscle
(1)
25. What is one of the mechanisms that provide increased termogenezei in fever?
3. Boost lipolizei and glicogenolizei
(3)
26. C has is one of the mechanisms that provide increased termogenezei in fever?
2. Hipersecreţia catabolizanţi hormones
(2)
27. C has is one of the mechanisms that provide increased termogenezei in fever?
5. The contraction of skeletal muscle clinic
(5)
28. C has the mechanisms that provide increased termogenezei in fever?

6. Boost lipolizei and glicogenolizei
(1.5)
29. C has the mechanisms that provide increased termogenezei in fever?
11. Hipersecreţia catabolizanţi hormones
(1.5)
30. What is one of the mechanisms of reducing termolizei in the period of foot?
1. Skin vessels Spasm
2. increased sweating
3. retention of urine
4. the spasm of abdominal organs
5. skeletal muscle vessels spasm
(1)
1. Decrease sudoraţiei
(1)
1. Pulmonary Hipoventilaţie
(1)
33. What are the mechanisms of reducing termolizei in the period of foot?
10. Skin vessels Spasm
(1.5)
34. What are the mechanisms of reducing termolizei in the period of foot?
15. Decrease sudoraţiei
(1.5)
35. what temparatură of the body is maintained in subfebrile reactions?

1. 36.9-38,0C
2. 38,1-39C
3. 39.1-40C
4. more top 40,1C
5. 36.4-36.9C
(1)
36. what temparatură of the body keep in hiperpiretice reactions?

1. above 38,0C
2. above 39C
3. above 40C
4. above 41C
5. above 42C
(4)
37. what temperature fever dangerous for the body?

1. 36.9-38,0C
2. 38,1-39C
3. 39.1-40C
4. more top 40,1C
5. 36.4-36.9C
(4)
38. How do I change the endocrine glands secretion during the State of the foot?
1. hipersecreţia corticotropinei and glucocorticoizilor
2. thyroid hiposecreţia
3. hipersecreţia insulin
4. hiposecreţia glucagonului
5. hiposecreţia mineralocorticoizilor
(1)
1. hipersecreţia of adrenal catecholamine
5. hiposecreţia mineraloorticoizilor
(1)
6. hipersecreţia of adrenal catecholamine
10. hipersecreţia corticotropinei and glucocorticoizilor
(1.5)
41. How do I change the function of cardiovascular system in the second period of foot?
1. tachycardia
2. generalized spasm of blood vessels
3. generalized vasodilation
4. "centralization" hemocirculaţiei
5. arterial collapse
(1)
4. hypertension
5. collapse
(4)
8. tachycardia
9. hypertension
10. collapse
(3,4)
44. How do I change the function of cardiovascular system in the third period of the foot?
1. bradycardia
3. vasodilation generalzată
5. hypertension
(3)
2. generalzată vasoconstriction
4. hypertension
5. low blood pressure
(5)
7. generalzată vasoconstriction
8. vasodilation generalzată
9. hypertension
(3.5)
47. How do I change the digestive system function in the foot?

1. hipersecrieţia digestive glands
2. intestinal hypermotility
3. intestinal atonie
4. diarrhea
5. gastric hypersecretion
(3)
3. hiposecrieţia digestive glands
4. diarrhea
(3)
3. Bowl fecal stagnation
4. diarrhea
(3)
6. intestinal atonie
9. diarrhea
(1.3)
1. hiposecrieţia digestive glands
(3,4)
52. what favourably has fever?

1. stimulate the processes of imunogeneză
2. inhibits allergic reactions
3. direct action bactericidal
4. accelerates regenerative processes
5. stimulates anabolic processes
(1)
53. what effect has a favourable fever?
1. stimulates phagocytosis
5. stimulates anabolic processes
(1)

2. direct action bacteriostatic
5. stimulates anabolic metabolic processes
(2)

3. potentiates the action of bacteriostatic antibioticilor
(3)
56. what favorable effects has a fever?

6. stimulate the processes of imunogeneză
(1.3)

11. stimulates phagocytosis
(1.3)

16. direct action bacteriostatic
(1.3)
STRESS
59. What is stress?

1. General non-specific reaction to any stimulus
2. the general reaction is specific to each exciting
3. complex compensatory reactions to any exciting
4. protective effects of any exciting
5. reparative complex reactions I any exciting
(1)
60. What is stress?
1. General compensatory reaction
2. General pathological reaction
3. General protective reaction
4. the general reaction reparative
5. the general reaction of adaptation
(5)
61. What is stress?

6. General non-specific reaction to any stimulus
7. General pathological reaction
8. General protective reaction
9. the general reaction reparative
10. the general reaction of adaptation
(1.5)
62. What is the reaction of the CNS in shock stage of stress?

1. simpato-adrenal system
2. enabling autonomic parasympathetic system
3. inhibition of cerebral cortex protective
4. the inhibition of the neuroendocrine hypothalamus
5. inhibition of reticular system
(1)
63. What is the reaction of the cardiovascular system in the phase of shock stress?
6. tachycardia
8. bradycardia
9. myocardial hypertrophy
10. circulatory failure
(1)
64. What is the reaction of the cardiovascular system in the phase of shock stress?
11. peripheral vasoconstriction
13. bradycardia
14. myocardial hypertrophy
(1)
65. What are side effects of cardiovascular system in the phase of shock stress?
16. peripheral vasoconstriction
18. bradycardia
19. tachycardia
(1.4)
66. What is the metabolic reaction in the shock stage of stress?

23. enhancement of anaerobic catabolism
24. intensifying cetogenezei
25. hypoglycemia
(1)
67. What is the reaction of the CNS in contraşoc stage of stress?

1. simpato-adrenal system
2. activation of the parasympathetic autonomic nervous system
26. inhibition of cerebral cortex protective
27. the inhibition of the neuroendocrine hypothalamus
3. inhibition of reticular system
(1)
68. What is the endocrine system reaction in contraşoc stage of stress?
1. hipersecreţia vasopressin from being
2. hiposecreţia vasopressin from being
3. activation of Renin-angiotensin-aldosterone
4. hipersecreţia thyroid hormones
(1)
71. what is the endocrine system reaction in stress resistance stage?

1. hipersecreţia and corticosuprarenalelor hypertrophy
(1)
1. corticosuprarenalelor atrophy
9. hiperecreţia vasopressin from being
(2)
2. glucocorticisteroizilor stagnation
3. hiposecreţia sexuaţi hormones
(3)
74. What are the reactions of the endocrine system in stress-resistance?
10. hipersecreţia and corticosuprarenalelor hypertrophy
(3.5)
75. What are the reactions of the endocrine system in stress-resistance?
15. hiperecreţia vasopressin from being
(3.5)
79. How do I change the biochemistry of blood in resistance to stress?

1. hyperglycemia
2. hypoglycemia
3. hipolipidemie
4. hyperammonaemia
5. hyperuricemia
(1)
1. hypoglycemia
2. Hyperlipidemia
3. hipolipidemie
4. hyperammonaemia
5. hyperuricemia
(2)

1. hypoglycemia
2. hipolipidemie
3. hiperazotemie
4. hyperammonaemia
5. hyperuricemia
(3)
1. hypoglycemia
2. hipolipidemie
3. hyperammonaemia
4. hperaminoacidemie
5. hyperuricemia
(4)
83. what biochemical changes occur in the blood at the stage of stress resistance?
6. hypoglycemia
7. hipolipidemie
8. hyperammonaemia
10. hyperglycemia
(4.5)
84. The biochemical changes occur in the blood at the stage of stress resistance?
11. hypoglycemia
12. hipolipidemie
13. hyperammonaemia
15. hiperazotemie
(4.5)
85. what biochemical changes occur in the blood at the stage of stress resistance?
16. hypoglycemia
17. hipolipidemie
18. hyperammonaemia
20. Hyperlipidemia
(4)
86. What is stress exhaustion stage?

2. hipersecreţia glucocorticoizilor
4. corticosuprarenalelor hyperplasia
5. hyperthermia
(1)
87. What is stress exhaustion stage?
1. hiposecreţia glucocorticoizilor
4. corticosuprarenalelor hyperplasia
5. hyperthermia
(1)
88. What is manifested in the stress exhaustion stage?

1. hipoptermie
2. hyperthermia
3. Decompensated alkalosis
4. obesity
5. predominance of the anabolism of catabolism
(1)
89. What is manifested in the stress exhaustion stage?
1. hyperthermia
2. Decompensated acidosis
4. obesity
(2)
90. What is the State of exhaustion in stress?
1. hyperthermia
3. caşexie
4. obesity
(3)
91. What is manifested also in stress exhaustion stage?
1. hyperthermia
3. depletion of glycogen and lipids
4. obesity
(3)
6. hyperthermia
(3,4)
11. hyperthermia
14. hiposecreţia glucocorticoizilor
(3,4)
16. hyperthermia
19. hipoptermie
(3,4)
21. hyperthermia
24. Decompensated acidosis
(3,4)
26. hyperthermia
29. caşexie
(3,4)
102. What is possible in the complication of stress Burnout?

1. anemia
2. Leukocytosis
3. lymphoid tissue hyperplasia
4. obesity
5. hypertension
(1)
1. Leukocytosis
2. osteoporosis
4. obesity
5. hypertension
(2)
1. Leukocytosis
3. immunodeficiency
4. obesity
5. hypertension
(3)
1. Leukocytosis
3. predisposition to allergic reactions
4. obesity
5. hypertension
(3)
1 ' 06. What is the complication of stress exhaustion stage?
1. Leukocytosis
3. caşexie
4. obesity
5. hypertension
(3
1. Leukocytosis
3. obesity
4. gastric and duodenal ulceration
5. hypertension
(4)

1. Leukocytosis
3. obesity
4. atrophy of lymphoid tissue
5. hypertension
(4)
109. What are possible complications in stress exhaustion stage?
6. Leukocytosis
8. anemia
10. hypertension
(3,4)
11. Leukocytosis
13. osteoporosis
15. hypertension
(3,4)
16. Leukocytosis
18. immunodeficiency
20. hypertension
(3,4)
21. Leukocytosis
23. predisposition to allergic reactions
25. hypertension
(3,4)
26. Leukocytosis
28. caşexie
30. hypertension
(3,4)
31. Leukocytosis
33. gastric and duodenal ulceration
35. hypertension
(4)
7. ALLERGY (93)
1. what immunological processes underlying allergic reactions immediate type?

1. humoral immune reactions of the type
2. immune reactions of the cell type
3. acute inflammation
5. immunodeficiencies
(1)
2. what immunological processes underlying allergic-type reactions delayed?

1. humoral immune reactions of the type
2. immune reactions of the cell type
5. immunodeficiencies
(2)
3. How is the type I allergic reactions (anaphylactic)?

1. the reaction between antibody and allergen drop parenchymal cells
2. the reaction of the allergen cell antibodies fixed on the movement
3. the reaction of both antibody and allergen in circulation
4. the reaction of the allergen and sensitized lymphocytes
5. the reaction between antibody and allergen drop on mast cells
(5)
4. What characterizes the allergic reactions of type II (cytotoxic)?

5. the reaction between antibody and allergen drop on mast cells
(2)
5. What characterizes the allergic reactions of type III (Arthus)?

5. the reaction of the allergen antibody in circulation and drop on mast cells
(3)
6. What characterizes the allergic reactions of type IV (delayed)

(4)
7. What is V-type allergic reactions (stimulator)?

2. the reaction of the cellular receptors and antibodies in circulation
(2)
8. how long does the anaphylactic reaction latent after first contact with the allergen?
1. a few minutes
2. a couple of hours
3. 5 days
4. 4 weeks
5. different, depends on the dose and type of Antigen
(3)
9. how much time it keeps the State of the active awareness of anaphylaxis?
1. 2 hours ago
2. 5 days
3. 14 days ago
4. 4 weeks
5. more than 6 months
(5)
10. what antigens causing anaphylactic allergic reactions?

1. hyperimmune sera
2. Mycobacterium
3. viruses
4. incompatible red cells
5. cellular transplantation
(1)
11. vaccines
12. Mycobacterium
13. viruses
(1)
1. antibiotics
2. Mycobacterium
3. viruses
(1)
1. pain killers
2. Mycobacterium
3. viruses
(1)

1. pain killers
6. Mycobacterium
7. viruses
8. hyperimmune sera
(1.4)
1. pain killers
10. Mycobacterium
11. viruses
1. vaccines
(1.4)
1. pain killers
13. Mycobacterium
14. viruses
1. antibiotics
(1.4)
16. What cell carries out anaphylactic allergic reactions?

1. macrofagii
2. B lymphocytes
3. mast cells
4. killer T cells
5. fibroblaştii
(3)
17. The immunoglobulins participates in anaphylactic allergic reactions?

1. immunoglobulin E
2. immunoglobulins G1
3. the immunoglobulin
4. immunoglobulin M
5. immunoglobulin D
(1)
18. Where are localized IgE in anaphylactic reactions?

1. circulates in the blood plasma
2. attached to mast cells
3. mounted on B-lymphocytes
4. fixed on T-lymphocytes
5. fixed endotelioicite
(2)
19. What is a mediator in mast cells in stored?

1. histamine
2. interleukins
3. leucotrienele
4. interferons
5. prostaglandins
(1)
20. what mediators are synthesized in mast cells on the ciclooxigenazică?

1. histamine
2. factroi chemotactici
3. activant factroul of platelet
4. leukotrienes
5. prostaglandins
(5)
21. what mediators are synthesized in mast cells on the lipooxigenazică?
1. histamine
2. factroi chemotactici
3. activant factroul of platelet
4. leukotrienes
5. prostaglandins
(4)
22. What is one of the pathophysiological processes local in anaphylactic reactions?

1. chronic proliferative inflammation
3. atrophy
4. hyperplasia
5. muscular dystrophy with lipids
(2)
23. what process pathophysiology develops in the lungs in anaphylactic reactions?

1. bronchospasm
2. atelectasis
3. parenchymal inflammation
4. cor pulmonale
5. myocardial
(1)
24. what process pathophysiology develops in the cardiovascular system in anaphylactic
reactions?
1. hypertensive crisis
2. arterial collapse
3. cor pulmonale
4. increase the heart's postsarcina
5. increase code presarcina
(2)
25. what process pathophysiology develops in the digestive tract in anaphylactic reactions?
1. smooth muscle atonia
2. smooth muscle spasm
3. constipation
4. gastric chimostaza
5. flatulence
(2)
26. How long does it take hiposensibizare period after anaphylactic shock?
1. a few minutes
2. a couple of hours
3. 2ăptămâni
4. 6 months
5. all subsequent life
(3)
27. what antigens involved in allergic reactions type II (cytotoxic, citolitice)?
1. microbial antigens associated to plasma proteins
2. normal antigens from mutant cells
3. eritrocitare antigens in association with exogenous haptenele
4. sequestered antigens of the lens, the testicles, myelin
5. exogenous antigens attached to body cells
(3)
3. leucocites number antigens in association with exogenous haptenele
4. sequestered antigens of the lens, the testicles, the myelin
(3)

3. antigens, recovered in association with haptene
(3)

3. izoantigenele eritrocitare
(3)
6. eritrocitare antigens in association with exogenous haptenele
(2,3)
10. leucocites number antigens in association with exogenous haptenele
(2,3)
14. antigens, recovered in association with haptene
(2,3)
34. What is the mechanism of cytolisis in allergic reactions type II (cytotoxic, citolitice)?
1. distrucţia own cells directly by antibodies
2. distrucţia own cells directly by macrofagi
3. distrucţia own cells directly by B lymphocytes
4. distrucţia direct the cells of complement C5-enabled
5. phagocytosis cells opsonizate with C9 and Fab
(4)
35. What is the mechanism of cytolisis in allergic reactions type II (cytotoxic, citolitice)?
1. direct distrucţia own cells by antibodies
3. distrucţia own cells directly by B lymphocytes
4. phagocytosis of opsonizate cells C9 and Fab
5. phagocytosis of opsonizate cells C3b and Fc
(5)
36. What are the mechanisms of cytolisis in allergic reactions type II (cytotoxic, citolitice)?
1. direct distrucţia own cells by antibodies
7. distrucţia own cells directly by C5-9 of activated complement
8. phagocytosis of opsonizate cells C9 and Fab
9. phagocytosis of opsonizate cells C3b and Fc
(3.5)
37. What is type II clinical allergic reactions?

1. eritrocitopenie
2. absolute eritrocitoză
3. relative eritrocitoză
4. megaloblastic
5. iron deficiency anemia
(1)
1. Leukocytosis eozinofilă
2. leucocitopenie neutrofilă
3. acute leukemia
4. limfocitopenie
5. chronic leukemia
(2)
1. trombocitoză
2. trombocitopatie
3. thrombocytopenia
4. trombogeneza
5. disseminated intravascular coagulation
(3)
1. anaphylactic shock
2. shock hemotransfusional
3. hemorrhagic shock
5. serum sickness
(2)

9. eritrocitopenie
(2.5)
13. leucocitopenie neutrofilă
(2.5)
17. thrombocytopenia
(2.5)
44. what antigens initiates an allergic reaction type III?

1. hyperimmune sera
2. antibiotics
3. autoantigenele
4. the pollen plant
5. contact antigens
(1)
45. under what conditions is allergic reaction type III?

1. Antigen-antibody against excesivitatea
2. the formation of immune complexes, which complement and stimulate fagocitaţi
3. massive haptene administration
4. type humoral immunodeficiency
5. type cellular immunodeficiency
(1)
1. the formation of immune complexes activate complement not in blood
2. the formation of immune complexes and complement are launched fagocitaţi
5. mixed type of immunodeficiency
(1)
1. formation of immune complexes that activate complement and are fagocitaţi
3. depletion of complement
(3)
1. immune complex with high molecular mass, which activates complement and are
fagocitaţi
3. hereditary defects of the complement
(3)
fagocitaţi
4. immune compound with low molecular mass, which infiltrate the vascular wall and
interstiţiul
(4)
fagocitaţi
4. hiperpermeabilitatea vascular wall
(4)
fagocitaţi
9. Antigen-antibody against excesivitatea
(4.5)
fagocitaţi
13. the formation of immune complexes activate complement not in blood
(4.5)
fagocitaţi
17. depletion of complement
(4.5)
fagocitaţi
21. hereditary defects of the complement
(4.5)
fagocitaţi
25. immune compound with low molecular mass, which infiltrate the vascular wall and
interstiţiul
(4.5)
56. What is one of the mediators of allergic reaction type III?

1. snippets complement C3a, C4a, enabled C5a
2. limfokinele
3. perforina
4. interferons
5. activated complement C5 snippets-9
(1)
2. limfokinele
3. perforina
4. interferons
(1)
1. mastocitari mediators
2. limfokinele
3. perforina
4. interferons
(1)
1. prostaglandins
2. limfokinele
3. perforina
4. interferons
(1)
60. What are mediators of allergic reaction type III?
1. prostaglandins
6. limfokinele
7. perforina
8. snippets complement C3a, C4a, enabled C5a
(1.4)
61. What are the mediators of allergic reaction type III?
1. prostaglandins
10. limfokinele
11. perforina
(1.4)
62. What are the mediators of allergic reaction type III?
1. prostaglandins
14. limfokinele
15. perforina
16. mastocitari mediators
(1.4)
63. What structures are allergic reactions affect the type III?
1. the wall of blood vessels
2. the myocardium
3. the liver
4. striated muscles
5. brain
(1)
64. What structures it affects type III allergic reactions?
1. basal membrane endothelial
2. the myocardium
3. the liver
4. striated muscles
5. brain
(1)
1. renal glomerulul
2. the myocardium
3. the liver
4. striated muscles
5. brain
(1)
1. grants the joints
2. the myocardium
3. the liver
4. striated muscles
5. brain
(1)
6. the myocardium
7. the liver
8. striated muscles
9. the wall of blood vessels
(1.5)
10. the myocardium
11. the liver
12. striated muscles
1. renal glomerulul
(1.5)
13. the myocardium
14. the liver
15. striated muscles
1. basal membrane endothelial
(1.5)
70. what cells are often included in V-type allergic reactions?

1. tirocitele
2. adipocitele
3. ribbed miocitele
4. endoteliocitele
5. neuron
(1)
71. What are mediators of allergic reactions patochimice phase type IV?
1. prostaglandins
2. histamine
3. leukotrienes
4. serotonin
5. limfotoxinele
(5)
72. What are the mediators of allergic reactions patochimice phase type IV?
6. prostaglandins
7. histamine
8. leukotrienes
9. serotonin
(5)
1. prostaglandins
2. histamine
3. leukotrienes
4. serotonin
5. chimiotactic of mononuclearilor factor
(5)
74. What are the mediators of allergic reactions patochimice phase type IV?
1. prostaglandins
2. histamine
3. leukotrienes
4. serotonin
5. limfokine
(5)
6. prostaglandins
7. histamine
8. leukotrienes
9. limfotoxinele
10. limfokine
(4.5)
11. prostaglandins
12. histamine
13. leukotrienes
15. limfokine
(4.5)
16. prostaglandins
17. histamine
18. leukotrienes
19. chimiotactic of mononuclearilor factor
20. limfokine
(4.5)
78. What is the final manifestation of the allergic type reactions IV?
1. exsudativă inflammation with purulent abscess formation
2. fibrinous inflammation difteritică
3. proliferative inflammation with formation of granulomului
4. hiperegică inflammation with necrosis with scarring
5. alterativă inflammation with necrosis with scarring
(3)
79. What is non-specific hypersensitivity?
1. delayed type allergic reaction
2. immediate type allergic reactions I
3. inflammatory reaction caused by activated complement on the classical pathway
4. inflammatory reaction caused by nonspecific activation of macrfoifagilor
5. inflammatory reaction caused by non-specific ' degranulation of mast cells
(5)
3. inflammatory reaction caused by unauthorized activated complement
5. inflammatory reaction caused by nonspecific activation of macrfagilor
(3)

3. inflammatory reaction caused by activated complement alternative pathway
5. leucotrienelor reaction caused by excess and deficiency of prostaglandins
(5)

1. hypersensitivity caused by antigen immunological phase; include patochimică, and
fiziopatologică
2. inflammatory reaction caused by non-specific ' degranulation of mast cells
3. hypersensitivity caused by factors nonantigenici; include immunological phase and
fiziopatologică
patochimică
5. hypersensitivity caused by factors nonantigenici; patochimică and fiziopatologică phase
contains
(2.5)
fiziopatologică
7. inflammatory reaction caused by unauthorized activated complement
fiziopatologică
patochimică
contains
(2.5)
fiziopatologică
12. leucotrienelor reaction caused by excess and deficiency of prostaglandins
fiziopatologică
patochimică
contains
(2.5)
85. what processes include nonspecific hypersensitivity?

16. imunoligic stage patochimic stage;; stage pathophysiology
17. imunoligic stage patochimic stage;;
18. stage imunoligic stage pathophysiology;
19. stage patochimic stage pathophysiology;
20. progress in pathophysiology
(4)
86. What is the cause of autoimmune reactions?

1. the lack of immunological tolerance to self antigens, native
2. immunocompetent cell allogeneic transplantation
5. hereditary defects in the complement system
(1)
1. modifying your own antigens under the action of physical factors
(1)

1. Association of microorganisms to own antigens
(1)
89. what causes the autoimmune reactions?
10. the lack of immunological tolerance to self antigens, native
(1.5)
90. what causes the autoimmune reactions?
15. modifying your own antigens under the action of physical factors
(1.5)
91. What is the consequence of development of autoantibodies against tireoglobulinei?

1. thyroid necrosis
2. atrophy of the thyroid
3. hipersecreţia of thyroid hormones
4. hiposecreţia of thyroid hormones
5. thyroid cancerizarea
(4)
92 Which is the consequence of development of autoantibodies against antianemic intrinsic

factor?
1. ciancobalaminei deficiency
2. iron deficiency
3. eritropoietinelor failure
4. low ferritin
5. isuficienţa transferrin
(1)
93. What are the consequences of postsinaptici receptor antibodies to miocitului striated?
the nonspecific activation and tonic muscle contractions
the nonspecific activation and clonice muscle contractions
cholinesterase activity loss and tonic muscle contractions
blocking receptors and muscle paralysis
blocking the intracellular cAMP and muscle paralysis
(4)
8. MICROCIRCULATION (113)
1. What is the main pathogenetic link hiperemiei pressure?
1. increase cardiac output
2. Reduceeai high tide of blood through the veins
3. Creşteeai influx of blood through dilated arteries
4. Increasing the influx of blood through dilated tiny arterioles
5. Increased systemic blood pressure
(4)
2. What is the correlation between the inflow and outflow of blood in hyperemia pressure?
1. the inflow and outflow are reduced proportionately
2. the influx of low tide predominates
3. the inflow and outflow are increased in proportion
1. Prevailing over the low tide and Ebb
2. The inflow and outflow will be kept at the level originally
(3)
3. What is the mechanism of pathogenesis of arterial hiperemiei type neurotonic?

1. Decrease of vascular tone
2. Increased sympathetic tone and Autonomic system
3. Creşteeai parasympathetic autonomic system tone
4. Reduction of the autonomic system, sympathetic tone
5. Reduction of vascular reactivity to acetylcholine.
(3)
4. What is the mechanism of pathogenesis of arterial neuroparalitic type hiperemeia?

1. Primary vascular tone Micşorrea
2. Reducing sympathetic influences asipra dish
3. Autonomic system sympathetic tone Growth
4. Increased parasympathetic autonomic system tone
5. Reduction of asipra vessel parasympathicus influences
(2)
5. What is the mechanism of pathogenesis of hiperemiei material neuromioparalitice?

1. Depletion of catecholamine nerve blister terminaţiunilor cute
2. Increased parasympathetic autonomic system tone
3. action gangloblacatorilor
4. severing the nerves of fun
5. Prolonged Compression on vessels
(1)
6. What is the mechanism of pathogenesis of arterial hiperemiei functional?

1. Metabolic
2. endocrine
3. humoral
4. Neurotonic
5. neuroparalitic
(1)
7. What is hyperemia pressure?
1. Hydrostatic pressure Increase of the blood in the arteries
2. Hydrostatic pressure Increases the blood in the veins
3. Increasing the speed of linear and volumetric blood torentului
4. Hypoperfusion
5. Limfogenezei Reduction
(3)
6. Hydrostatic pressure Increase of the blood in the arteries
7. Hydrostatic pressure Increases the blood in the veins
8. Capillary hydrostatic pressure rise
9. Hypoperfusion
10. Limfogenezei Reduction
(3)

1. Cyanosis due to the accumulation of hemoglobin neoxigenate
2. Cyanosis due to accumulation of carbohemoglobinei
3. the redness caused by accumulation of oxihemoglobină
4. the redness caused by accumulation of free oxygen
5. the redness caused by accumulation of methemoglobinei
(3)
1. Lowering the temperature caused by dwindling local metabolism and termogenezei
2. Lowering the temperature increase caused by the local termolizei local
3. Local temperature rise caused by increasing metabolism and termogenezei
4. Local temperature rise caused by General hiperztermia fever
5. Local temperature rise caused by hyperactivity of the hiperemiat
(3)

1. Increasing the amount of interstitial fluid with intensifying limfogenezei
2. Increasing the amount of interstitial fluid due to the decrease in rezorbţiei liquid
intzerstiţial
3. Increasing the amount of interstitial fluid due to compression of the lymphatic vessels
4. Increasing the amount of interstitial fluid due to increased capillary permeability
5. Increasing the amount of interstitial fluid due to reduction of limfogenezei
(1)

intzerstiţial
10. Increasing the speed of linear and volumetric blood torentului
(1.5)
intzerstiţial
the redness caused by accumulation of oxihemoglobină
(1.5)
intzerstiţial
Capillary hydrostatic pressure rise
(1.5)
intzerstiţial
Local temperature rise caused by increasing metabolism and termogenezei
(1.5)
17. What is the venous hyperemia?

1. Overfilling with blood body due to increased inflow
2. Overfilling with blood body due to restricted blood at low tide
3. Overfilling with blood because of a reduction in the blood at low tide
4. Overfilling with blood due body hipervolemiei
5. Overfilling with blood body due to the increase of central venous pressure
(3)
18. What is the cause of venous hiperemiei?

1. artery Compression
Compesia vein
Decreasing parasympathetic autonomic system tone
Increasing the flexibility of the venous wall
hiperhidratarea-General
(2)
1. artery Compression
Increasing the flexibility of the vein wall
The right ventricle of the heart failure
(4)
Artery compression
Insufficiency of left ventricle of heart
(5)
Artery compression
General hiperhidratarea
Vein valve insufficiency
(5)

Artery compression
General hiperhidratarea
1. Portal vein Obstruction
(5)
Artery compression
Compesia vein
(2.5)
Artery compression
The right ventricle of the heart failure
(2.5)
Artery compression
Insufficiency of left ventricle of heart
(2.5)
Artery compression
Vein valve insufficiency
(2.5)
27. What is the pathogenic linkthe main part of the venous hiperemiei?
1. Increasing the gradient of pressure artery-vein
2. Reducing venous low tide
3. Arterilolelor Spasm
4. Decrease in intrathoracic pressure
5. venulelor palsy
(2)
28. What are the external manifestations of venous hiperemiei?

1. Diffuse Erythema, edemaţiere and local temperature decrease
2. Diffuse Erythema, edemaţiere and local temperature rise
3. Cyanosis, swelling and increased local temperature
4. Cyanosis, edemaţiere and local temperature decrease
5. Pallor, swelling and decrease local temperature
(4)
29. What is the cause of increasing the volume of venous hyperemia in body?
1. adipose tissue growth
2. Edema
3. scar tissue organ
4. Hypertrophy
5. Hyperplasia.
(2)
30. What is the cause of local temperature decrease in venous hyperemia?

1. termolizei local growth
2. General Hypothermia
3. Reducing venous blood at low tide
4. Reduction of tissue metabolism
5. reducing local termolizei
(4)
31. what consequences lead venous hyperemia?

1. Cellular Damage
2. Hypertrophy
3. Hyperplasia
4. dediferenţierea
5. fat dystrophy
(1)
44. what consequences result From venous hyperemia?
1. Necrosis
2. Hypertrophy
3. Hyperplasia
4. dediferenţierea
5. fat dystrophy
(1)
1. Atrophy
2. Hypertrophy
3. Hyperplasia
4. dediferenţierea
5. fatty dystrophy
(1)
1. Scar Tissue
2. Hypertrophy
3. Hyperplasia
4. dediferenţierea
5. fat dystrophy
(1)
1. inflammation
2. Hypertrophy
3. Hyperplasia
4. dediferenţierea
5. fat dystrophy
(1)
1. inflammation
6. Hypertrophy
7. Hyperplasia
8. dediferenţierea
9. Cellular Damage
(1.5)
1. inflammation
10. Hypertrophy
11. Hyperplasia
12. dediferenţierea
1. Necrosis
(1.5)
1. inflammation
13. Hypertrophy
14. Hyperplasia
1. Atrophy
(1.5)
. What consequences result from venous hyperemia? 38
1. inflammation
16. Hypertrophy
17. Hyperplasia
1. Scar Tissue
(1.5)
39. pathogenetic mechanisms of ischemia?

1. obturation, obliteration veins, compression
1. venodilataţia, constricting arteries, capillaries spasm
2. knockout, compression, artery obliteration
3. the spasm of capillaries and venulelor
4. dilation of the arteries, capillaries and venulelor
(3)
40. how to change local hemodynamics in ischemia?

1. Reducing capillary as urolithiasis
2. Hiperperfuzie
3. Intrensificarea limfogenezei
4. Blood linear velocity Growth
5. Increased volumetric rate of blood
(1)
1. Decrease in blood volume speed
2. Hiperperfuzie
3. Intrensificarea limfogenezei
(1)
6. Decrease in blood volume speed
7. Hiperperfuzie
8. Reducing capillary as urolithiasis
(1.3)
43. How do I change cell metabolism in ischemiie?

1. reduction of oxidative processes
2. Gaseous Acidosis
3. oxidative processes intensiificarea
4. enhancing the anabolic processes
5. intensifying glicogenogenezei
(1)
1. enhancement of anaerobic processes
2. Gaseous Acidosis
(1)
1. metabolic acidosis
2. Gaseous Acidosis
(1)
1. reduction of ATP synthesis
2. diminishing the use of ATP
(1)
1. increased synthesis of lactic acid
2. increased uric acid acid synthesis
(1)
9. reduction of oxidative processes
(1.4)
enhancement of anaerobic processes
(1.4)
metabolic acidosis
(1.4)
reduction of ATP synthesis
(1.4)
52. Through what manifests outward ischemia?

1. Diffuse Erythema
2. Tissue Swelling
3. Paresthesia, pain
4. Skin turgescence Growth
5. Cyanosis
(3)
53. What is manifested outwardly ischemia?
1. Diffuse Erythema
2. Tissue Swelling
3. Local temperature Decrease
5. Cyanosis
(3)
1. Diffuse Erythema
2. Tissue Swelling
3. Pallor
5. Cyanosis
(3)
1. Diffuse Erythema
2. Tissue Swelling
3. Decrease in skin turgor alterations
5. Cyanosis
(3)
56. Which are the manifestations of ischemia?

6. Diffuse Erythema
7. Paresthesia, pain
10. Cyanosis
(2,3)
57. What are the manifestations of ischemia?
11. Diffuse Erythema
12. Local temperature Decrease
15. Cyanosis
(2,3)
58. Which are the manifestations of ischemia?
16. Diffuse Erythema
17. Pallor
20. Cyanosis
(2,3)
59. what organ colateralele are absolutely insufficient functional?

1. lower limbs
2. upper limbs
3. Live
4. lungs
5. myocardium
(5)

1. lower limbs
2. upper limbs
3. Live
4. lungs
5. brain
(5)
1. lower limbs
2. upper limbs
3. Live
4. lungs
5. kidney
(5)
62. what organs are absolutely insufficient functional colateralele?
6. lower limbs
7. myocardium
8. Live
9. lungs
10. kidney
(2.5)
63. what organs are absolutely insufficient functional colateralele?
11. lower limbs
12. brain
13. Live
14. lungs
15. kidney
(2.5)
64. What is endogenous embolism?

1. Ateromatoasă
1.gaseous form
2.bacterial
3.with the larvae of parasites
4.with the bacteria in the digestive tract
(1)
5.Trombembolia
6.gaseous form
7.bacterial
8.with the larvae of parasites
9.with the bacteria in the digestive tract
(1)
10. with lipids
11. gas
12. bacterial
13. the larvae of parasites
14. the bacteria in the digestive tract
(1)
15. with amniotic fluid
16. gas
17. bacterial
(1)
21. gas
22. bacterial
1. Ateromatoasă
(1.4)
25. gas
26. bacterial
27. Trombembolia
(1.4)
30. gas
31. bacterial
32. with lipids
(1.4)
71. What is exogenous embolism?

1. Ateromatoasă
2. Trombembolia
3. with lipids
5. gaseous form
(5)
1. Ateromatoasă
5. Trombembolia
6. with lipids
2. by air
(5)
1. Ateromatoasă
2. Trombembolia
3. with lipids
3. bacterial
(5)
1. Ateromatoasă
2. Trombembolia
3. with lipids
(5)
1. gas 5.
2. Trombembolia
3. with lipids
(1.5)
6. 1. air
2. Trombembolia
3. with lipids
(1.5)
8. 1. bacterial
2. Trombembolia
3. with lipids
(1.5)
78. The căriu vessel trauma is possible air embolism?

1. The Aorta
2. Carotid Artery
3. Pulmonary Artery
4. hemoraoidale veins
5. Jugular Veins
(5)
1. The Aorta
2. Carotid Artery
3. Pulmonary Artery
5. subclaviculare vein
(5)
6. The Aorta
7. Carotid Artery
8. Pulmonary Artery
10. Cranial venous Sinus
(5)
81. The trauma which air embolism is possible on vessels?

11. Jugular Veins
12. Carotid Artery
13. Pulmonary Artery
(1.5)
82. The trauma which air embolism is possible on vessels?
16. subclaviculare vein
17. Carotid Artery
18. Pulmonary Artery
(1.5)
83. In the case of gas embolism occurs?

1. stay in terms of atmospheric hiperbarie
2. stay in terms of atmospheric hipobarie
3. quick changeover from normal pressure at hiperbarie
4. rapid transition from hipobarie to hiperbarie pressure
5. rapid transition from hiperbarie to normobarie
(5)
84. The vessel must be in case of the amniotic fluid embolism?

1. Uterine Veins
2. Coronary artery Branches
3. Pulmonary artery branches
4. The arteries of the uterus
5. The winery.
(3)
85. What are the consequences of the artery embolism?

1. Ischemia
3. Venous Stasis
4. venous hyperemia
5. capillary stasis
(1)
86. what factor blood rheological properties damaged?

1. increased hematocrit
2. decrease in hematocrit
3. decrease in erythrocyte sedimentation rate
4. prostaciclinele
5. proastaglandinele PGF 2
(1)
2. increased erythrocyte sedimentation rate
4. prostaciclinele
(3)
3. tromboxanii
4. prostaciclinele
(3)
89. what damage factor blood rheological properties?
3. prostaciclinele
4. activant of platelet factor
(4)
90. what factors deteriorating rheological properties of blood?

6. increased hematocrit
8. prostaciclinele
(1.4)

13. prostaciclinele
(1.4)
16. tromboxanii
18. prostaciclinele
(1.4)
9. PATHOPHYSIOLOGY of METABOLIC HIDROSALIN (51)
1. (1) how do I change osmolaratatea, protein and sodium levels in the blood to the
imprisonment of drinking water?
1. Hiperosmolaritate, hiperproteinemie, hipernatriemie.
2. Hiperosmolaritate, hiperproteinemie, hiponatriemie
3. Hypo, hypoproteinemia, hiponatriemie.
4. Hipoosmolaritate, hiperproteinemie, hiponatriemie
5. Izoosmolaritate, hiperproteinemie, hipernatriemie.
2. (1) how do I change osmolaratatea, sodium and protein content in the blood sweating?
1. Hiperosmolaritate, hiperproteinemie, hipernatriemie.
2. Hiperosmolaritate, hiperproteinemie, hiponatriemie
3. Hypo, hypoproteinemia, hiponatriemie.
4. Hipoosmolaritate, hiperproteinemie, hiponatriemie
5. Izoosmolaritate, hiperproteinemie, hipernatriemie.
3. (1) how do I change osmolaratatea, content of chlorine and hydrogen ions in the blood in
vomiting incoiercibilă?
1. Hiperosmolaritate, hipocloremie,lcaloză
2. Hiperosmolaritate, hipocloremie,cidoză.
3. Hypo-, hipocloremie,cidoză
4. Hypo-, hipocloremie,lcaloză.
5. Izoosmplaritate, hipercloremie, alkalosis
4. (1) how do I change osmolaratatea, contents of sodium and hydrogen ions in the blood in
diarrhea?
1. Izoosmolaritate, hiponatriemie,cidoză.
2. Hiperosmolaritate, hipernatriemie,lcaloză
3. Hypo-, hiponatriemie,cidoză
4. Hypo-, hiponatriemie,lcaloză.
5. Izoosmolaritate, hipernatriemie, alkalosis
5. (5) How do I change osmolaratatea, sodium, protein and potassium in the blood in
combustionit grade II-III?
1. Hypo, hiponatriemie, hypokalemia, hypoproteinemia.
2. Isoosmolaritate, hiponatrimie, hypoproteinemia hyperkalaemia.
3. Izoosmolaritate, hiponatrimie, hypoproteinemia, hiperkaliemiee
4. Hiperosmolaritate, hipernatriemie,ipoproteinemie, hyperkalaemia
5. Hiperosmolaritate, hiponatriemie, hypoproteinemia, hyperkalaemia
6. (5) how do I change the osmolarity, concentration of sodium and blood volume in acute
hemorrhage in the first 2 hours ?
1. Hypo, hiponatriemie, hypovolemic.
2. Hypo, hipernatriemie, hypovolemic
3. Hiperosmolaritate, hipernatriemie, hypovolemic
4. Izoosmolaritate, normoproteinemie, normovolemie
5. Izoosmolaritate, normoproteinemie, hypovolemic
7. (5) how do I change the volume of the blood cell concentration in the dehydration of
intravascular?
1. Hypovolemic, hemodiluţie, oligocitemie
2. Hypovolemic, hemoconcentrayou, policitemie
3. Hipavolemie, hemodiluţie, policitemie
4. Hipavolemie, hemconcentration, oligocitemie
5. Hipovolemie,emotionalstrength, policitemie
8. (1) what is the reaction of the countervailing charge in the disseminate tissue
dehydration?
1. Hipersecreţia aldosteronului
2. hiposecreţia aldosteronului
4. hiposecreţia Renin
5. hipersecreţia natriuretic hormone
9. (2) what is the reaction of the countervailing charge in the disseminate tissue
dehydration?
2. Vasopressin from being Hipersecreţia.
4. hiposecreţia Renin
10. (4) Which is the reaction of the countervailing charge in the disseminate tissue
dehydration?
3.hormoniului natriuretic hipersecreţia
4.Hiposecreţia natriuretic hormone
5.Hiposecreţia Renin
dehydration?
1. increased reabsorption of ions of K
2.reabsorption of Na ions
3.Diminishing kidney as urolithiasis.
4.increase kidney as urolithiasis
5.increasing the secretion of Renin
dehydration?
6.hormoniului natriuretic hipersecreţia
7.Hipersecreţia Renin
8.Hiposecreţia Renin
dehydration?
1. predominance transcapilare over as urolithiasis accelerated resorption
2. balance between filtraţia transcapilară and accelerated resorption
9.rezorbţiei fluid interstitial to impugn filtration
10. generalized edema
11. dropsy
14. (3.5) Which are the reactions of severance in the disseminate tissue dehydration?
12. rezorbţiei interstitial fluid to impugn filtration
14. Hipersecreţia aldosteronului
17. Vasopressin from being Hipersecreţia.
18.
21. Hiposecreţia natriuretic hormone
24. Diminishing the kidney as urolithiasis.
18. (3.5) reactions are compensatory in intravascular dehydration?

27. Hipersecreţia Renin
19. (4) how do I change capilaro-interstitial and exchanged the interstice-cell in

izoosmolară dehydration?
1. Intravascular fluid Passage in particular, cellular hiperhidratarea
2. Intravascular fluid Passage in particular cellular dehydration;
3. the interstitial fluid passage in cell hiperhidratare;
4. The interstitial fluid Passage in normal cell volume;
5. The interstitial fluid Passage in cellular dehydration;
hipersmolară dehydration?
6. Intravascular fluid Passage in particular, cellular hiperhidratare
10. Intravscular liquid in the vessel Passage; nornal cell volume
hipoosmolară dehydration?
11. Intravascular fluid Passage in particular, cellular hiperhidratare
15. The interstitial fluid Passage in normal cell volume;
22. (3) how do I change the volume, osmolarity of the blood, the concentration of sodium
and volume share of the excessive consumption of drinking water?
1. Hipervolemie; hiponatriemie; ratatinarea; hypo cells
2. Hipervolemie; hiperosmolaritate; hiponatriemie; ratatinarea the cells
3. Hypo-Hipervolemie;; hiponatriemie; cellular edema
4. Hipervolemie; hipersmolaritate; hiponatriemie; ratatinarea the cells
5. Hipervolemie; hierosmolaritate; hiponatriemie; cellular edema
23. (4) how do I change the volume of interstitial fluid and intracellular from excessive
consumption of drinking water?
1. interstitial dehydration; cellular edema.
2.interstitial cell dehydration dehydration;
3.interstitial hiperhidratare; normal intracellular volume
4.hiperhidratare interstitial cell edema;
5.exicoză cellular hiperhidratare interstitial;
24. (4) how do I change oncotică pressure and osmotic blood from the excessive
consumption of drinking water?
1. hipersmolaritate hipoonchie; .
2.normoosmolaritate hipoonchie;
3. thehypo-hipernchie;
4. thehypo-hipoonchie;
5.normoosmolaritate hiperonchie;
.
25. (2) how do I change oncotică pressure and osmotic blood to massive infusions of
isotonic NaCl solutions?
6.normoosmolaritate hipoonchie;
7.hypo-hiperonchie;
8.hipoonchie; hypo
9.normoosmolaritate hipernchie;
26. (3) how do I change the volume of interstitial fluid and intracellular at massive
infusions of isotonic NaCl solutions?
6.interstitial cell dehydration dehydration;
7.hiperhidratare normal intracellular volume interstitial;
8.hiperhidratare interstitial cell edema;
9.exicoză cellular hiperhidratare interstitial;
.
27. (2) Which are immediate changes in pressure and osmotic blood oncotice to massive
infusions of glucose 5%?
10. hipoonchie; normoosmolaritate
11. hypo-hiperonchie;
12. hypo-hipoonchie;
13. hipernchie; normoosmolaritate
28. (4) Which are late changes of pressure and osmotic blood oncotice to massive infusions
of glucose 5%?
14. hipoonchie; normoosmolaritate
15. hypo-hiperonchie;
16. hypo-hipoonchie;
17. hipernchie; normoosmolaritate
29. (3) what are the changes in the interstitial fluid volume immediate and massive
infusions of the intracellular solution glucose 5%?
10. interstitial cell dehydration dehydration;
11. hiperhidratare interstitial volume normal cellular;
12. hiperhidratare interstitial cell edema;
13. hiperhidratare interstitial cell exicoză;
30. (4) what are the changes in the interstitial fluid volume late and massive infusions of the
intracellular solution glucose 5%?
14. interstitial cell dehydration dehydration;
15. hiperhidratare interstitial; normal intracellular volume
16. hiperhidratare interstitial cell edema;
17. hiperhidratare interstitial cell exicoză;
31. (1) which is one ofeacţiile intravascular hiperhidratarea compensatory?

1. Hiposecreţia aldosteronului.
2. Activation of the Renin-angiotensin-aldosterone
4. hiposecreţia natriuretic hormone
5. hipersecreţia tireocalcitoninei
6. Vasopressin from being Hiposecreţia.

11. Hipersecreţia natriuretic hormone.

16. Increased Glomerular as urolithiasis.
21. Poliuria.
24. decrease in Glomerular as urolithiasis
25. oliguria
36. (1.5) Which are reacţiile intravascular hiperhidratarea compensatory?
26. Poliuria.
30. Hiposecreţia aldosteronului.

31. Poliuria.
35. Vasopressin from being Hiposecreţia.

36. Poliuria.
40. Hipersecreţia natriuretic hormone.

41. Poliuria.
45. Increased Glomerular as urolithiasis.
40. (1) what are the consequences of hiperhidratării hipoosmolare at the level of the cell?
1. Intracellular Edema.
2. Cell Dehydration
3. normohidriei preservation intracelulere
4. blocking the membrane water channel
5. Pumping ions of sodium in the interstice into cells
41. (1) The nimim edema?
1. The accumulation of fluid in the interstitium
2. The accumulation of fluid in the intracellular space
3. The accumulation of fluid in the well-known cavities
4. Fluid accumulation in the vascular bed
5. The accumulation of fluid in the brain ventricolele
42. (3) what is known as dropsy?

1. The accumulation of fluid in the interstitium.
2. The accumulation of fluid in the intracellular space.
3. The accumulation of transsudat in well-known cavities.
4. Accumulating effusions in well-known cavities.
5. Increasing the amount of liquid in the vascular bed
43. (2) what is the pathogenesis of cardiac oedema?

1. Hiperpermebilitatea of biological membranes
2. Hyperemia venoasă
3. Hipoproteinemia.
4. Hipernatriemia.
5. Limfostaza
7. secondary hiperaldosterinismul
8. Hipoproteinemia.
9. Hipernatriemia.
10. Limfostaza

12. activation of the Renin-angiotensin-aldosterone
13. Hipoproteinemia.
14. Hipernatriemia.
15. Limfostaza
46. (2.5) Which is cardiac oedema pathogenesis?
19. Hipernatriemia.
20. Hyperemia venoasă
47. (2.5) Which is cardiac oedema pathogenesis?

24. Hipernatriemia.
25. secondary hiperaldosterinismul
48. (4) what is the pathogenesis of nefritice oedema?

1. Hipoproteinemia
2. Hiperproteinemia
3. Venous Hyperemia
4. Activation of Renin-angiotensin system.
5. nefronului dystrophy
49. (4) what is the pathogenesis of nefrotice oedema?

2. Hipernatriemia.
3. Hiperazotemia.
4. Hipoalbuminemia.
5. Hipoglobulinemia
50. (4) Which is the pathogenesis of caşectice oedema?

2. Hipernatriemia.
3. tumor necrosis factor (caşexina)
4. Hipoproteinemia.
5. Albuminuria
51. (1) the pathogenesis of allergic oedema?

1. Hiperpermeabilizarea vessels
2. limfostaza
4. hipernatriemia
5. Hipoproteinemia.
10. PATHOPHYSIOLOGY of METABOLISM (205)
1. (1). Which product is formed from bacterial fermentation of carbohydrates in the

digestive tract?
1. Carbon dioxide.
2. Ethyl alcohol.
Acetic acid
butyric acid
pyruvic acid
2. (2). Which product is formed from the fermentation of carbohydrates bacterienă in the
digestive tract?
3. Ethyl alcohol.
4. Lactic acid.
5. Butyric Acid
6. acetric acid
7. pyruvic acid
3. (2,4). What products are formed from the fermentation of carbohydrates bacterienă in
the digestive tract?
8. Ethyl alcohol.
9. Lactic acid.
10. Acetic Acid
11. Carbon dioxide.
12. pyruvic acid
4. (2). What conditions promote bacterial fermentation the carbohydrates in the stomach?
1. Gastric Hiperaciditatea
2. gastric hipoaciditatea
3. Hiposalivaţia.
4. The lack of pepsinogenului in gastric juice
5. abundant secretion of gastric zaharidaze
5. (2). That is the consequence of fermentation of carbohydrates in the stomach?

1. The formation of biogenic amines
2. The accumulation of lactic acid.
3. Formation of hydrogen sulphide.
4. the formation of acetic acid
5. formation of pyruvic acid.
6. (2). That is the consequence of fermentation of carbohydrates in the stomach?

1. the formation of biogenic amines
2. The formation of carbon dioxide.
4. the formation of acetic acid
7. (2,4). What are the consequences fermentation of carbohydrates in the stomach?
6. The formation of carbon dioxide.
8. The accumulation of lactic acid.
8. (4). What is the cause of maldigestiei z aharidelor?

1. Insufficiency of salivary amylase.
2. Lack of hydrochloric acid in the stomach.
3. Insufficiency of gastric pepsin
4. Amylase pancreatic Insufficiency
5. dizaharidazelor pancreatic insufficiency
9. (4). What is the cause of maldigestiei z aharidelor?
1. Insufficient salivary amylase.
2. Insufficiency of clorhidri acid in the stomach.
3. Insufficiency of gastric pepsin
4. Insufficiency of intestinal dizaharidazelor
10 . (4.3). what causes maldigestiei zaharidelor?
1. Insufficient salivary amylase.
6. Insufficiency of clorhidri acid in the stomach.
7. Amylase pancreatic Insufficiency
8. Insufficiency of intestinal dizaharidazelor
11. (4). The case intensifies bacterial fermentation of carbohydrates in the large intestine?
1. urinary alkalinization intestinal environment
2. acidification of the intestinal environment
3. insufficiency of glicolitice enzymes in the large intestine
4. maldigestia and malabsorbţia of carbohydrates in the small intestine
5. Malabsorbţia carbohydrates in large intestine
12. (1). That is the consequence of fermentation glucidelor in thethick testinul?

1. Acidification of the intestinal environment
2. urinary alkalinization ntestinal environment
3. environmental ntestinal hipoosmolaritatea
4. Increased absorption of water from the large intestine
5. constipation
6. Environmental ntestinal Hiperosmolaritatea
10. Constipation
10. filtraţia water from the blood into the lumen of the small intestine bed
14. Constipation
14. gas formation
18. Constipation
18. Diarrhea.
22. constipation
16. (1,4). What are the consequences of fermentationglucidelor in thethick testinul?
22. Diarrhea.
25. Environmental ntestinal Hiperosmolaritatea
22. constipation
26. Diarrhea.
29. filtraţia water from the blood into the lumen of the small intestine bed
22. constipation
30. Diarrhea.
33. gas formation
22. constipation
19. (3). That is the consequence of the pulp in food ration deficiency the country?
1. Inhibition of growth of microflora.
2. The intensification of peristaltismului.
3. Intestinal Atonie
4. inaniţia glucidică
5. Diarrhea.
20. (3). What is the cause of malabsorbţiei monozaharidelor in the small intestine?
1. Hiposecreţia ball.
2. Gland Atrophy of the small intestine.
3. small bowel epithelium atrophy
4. pancreatic insufficiency
5. iron deficiency
21. (3). How do I change the contents of nutrients in the liver in inaniţia glucidică?
1. deficiency of glycogen and lipids
2. excess glycogen and lipid deficiency
3. glycogen deficiency and excess of lipids
4. excess glycogen and lipids
5. lack of glycogen and lipids
22. (3). How do I change the contents of nutrients in the blood in inaniţia glucidică?
1. hypoglycemia + hipolipidemie
2. the hyperglycemia + hipolipidemie
3. hypoglycaemia + Hyperlipidemia
4. the hyperglycemia + Hyperlipidemia
5. lack of glucose + hipolipidemie
23. (3). What is the reaction for compensatory normoglicemiei in inaniţia long-lasting?
1. the mobilization of glycogen in the liver
2. the mobilization of glycogen in muscles striated
3. gluconeogeneza of protein
4. gluconeogeneza of fatty acids
5. gluconeogeneza of ketone body substances
24. (2). How do I change the function in inaniţia glucidică endocrine glands?
1. hiperseceţia insulin
2. hiperseceţia glucocortocosteoizilor
3. hiposeceţia glucocorticosteroizilor
4. hiposeceţia glucagonului
5. thyroid hormone hipersecreţia
25. (4) which sources maintain blood sugar levels consistent with life in the long inaniţia?
1. the use of glycogen from the liver
2. conversion of fatty acids into glucose
3. the use of glycogen reserves of striated muscles
4. gluconeogeneza of amino acids
5. neosinteza glucose from acetyl CoA
26. (4) what are the sources of carbohydrates in endogenous inaniţia long glucidică?
1. Liver Glycogen.
2. Fatty acids from adipose tissue.
3. Plasma proteins.
4. Protein striated muscles
5. Striated Muscle Glycogen
6. Liver Glycogen.
8. Plasma proteins.
9. Connective tissue Proteins
11. Liver Glycogen.
13. Plasma proteins.
14. Lymphoid tissue Proteins
16. Liver Glycogen.
19. glycerol from lipoliză
30. (1.4) Which are sources of carbohydrates in endogenous inaniţia long glucidică?
21. Protein striated muscles
31. (1.4) Which are sources of carbohydrates in endogenous inaniţia long glucidică?
26. Connective tissue Proteins
32. (1,4) Which are sources of carbohydrates in endogenous inaniţia long glucidică?
31. Lymphoid tissue Proteins
33. (5) what is the mechanism of feeding for gluconeogenesis in the remains?
36. insulin-induced proteoliza
37. glucagon-induced proteoliza
38. proteoliza induced by thyroid hormones
39. proteoliza induced by pancreatic enzymes
40. proteoliza-induced glucocorticosteroizi
34. (5) Proteins which are subjected to organ catabolismului in inaniţia glucidică?
1. The Kidneys.
2. brain
3. plasma proteins
4. Myocardium.
5. striated muscles
35 . (5) Proteins which are subjected to organ catabolismului in inaniţia glucidică?
1. Kidneys.
2. brain
3. plasma proteins
4. Myocardium.
5. The Thymus.
36 . (2.5) the protein which organs are subject to catabolismului in inaniţia glucidică?
1. Kidneys.
6. striated muscles
7. plasma proteins
8. Myocardium.
9. The Thymus.
37. (5) Which is one of the possible consequences of intensifying the endogenous proteins in
gluconeogenezei?
1. kidney atrophy.
2. brain atrophy
3. hipoproteinemia
4. myocardial atrophy.
5. connective tissue atrofua
gluconeogenezei?
1. kidney atrophy.
6. brain atrophy
7. hipoproteinemia
9. osteoporosis
gluconeogenezei?
1. kidney atrophy.
10. brain atrophy
11. hipoproteinemia
gluconeogenezei?
1. kidney atrophy.
14. brain atrophy
15. hipoproteinemia
17. atrofua lymphoid tissue
41. (2.5) Which are the possible consequences of intensifying the endogenous protein
gluconeogenezei?
1. kidney atrophy.
18. atrofuaipoproteinemia connective tissue
gluconeogenezei?
1. kidney atrophy.
21. osteoporosis
22. hipoproteinemia
gluconeogenezei?
1. kidney atrophy.
26. hipoproteinemia
45. (2)what is the endocrine response to excessive consumption of carbohydrates?

1. Hipersecreţia insulin and glucagonului
2. Insulin and hiposecreţia glucagonului Hipersecreţia
3. Hiposecreţia insulin and glucagonului
4. Insulin and hipersecreţia glucagonului Hiposecreţia
5. Insulin and hipersecreţia glucocorticosteroizilor Hiposecreţia
46. (2) what is the endocrine response to excessive consumption of carbohydrates?

6. Hipersecreţia insulin and glucocorticosteroizilor
7. Insulin and hiposecreţia glucocorticosteroizilor Hipersecreţia
8. Hiposecreţia insulin and glucocorticosteroizilor
47. (5.2) What are the endocrine reacţiili from excessive consumption of carbohydrates?
11. Hipersecreţia insulin and glucocorticosteroizilor
12. Insulin and hiposecreţia glucagonului Hipersecreţia
13. Hiposecreţia insulin and glucocorticosteroizilor
15. hipersecreţia glucocorticosteroizilor
48. (1) the homeostatică reaction in hyperglycemia?

1. intensification of lipogenezei.
2. Intensifying lipolizei
3. intensifying glicogenolizei
4. transforming carbohydrates into amino acids
5. intensification of Glycolysis
1. Intensifying glicogenogenezei
6. Intensifying lipolizei
8. the transformation of carbohydrates in ainoacizi
9. intensification of Glycolysis
1. Hipersecreţia insulin.
2. hiposecreof insulin
4. intensifying lipolizei
5. Intensifying gluconeogenezei
51. (1.3) Which are homeostatic reactions in hyperglycemia?
1. intensification of lipogenezei.
52. (1.3) Which are homeostatic reactions in hyperglycemia?

1. Intensifying glicogenogenezei
53. (1) the glucozuriei mechanism is excessive consumption of carbohydrates?

1. race activity hexokinazei epithelium hyperglycemia renal
2. hyperglycemia inhibits activity hexokinazei renal epithelium
3. hyperglycemia leads to filtraţia of glucose in the kidney glomerulul
4. hyperglycemia in renal epithelium's ability compete to oxidize glucose
5. hyperglycemia in renal epithelium capacity race to synthesize glycogen
54. (3) what is the cause hypoglycaemia?

1. hipersecreţia corticotropinei
2. hiposecreţia insulin
3. Hiposecreţia glucocorticoizilor
4. hipersecreţia glucagonului
5. hipercecreţia catecholamine

3. Hipersecrteţia glucocorticoizilor
4. Renal Glucozuria
5. hipercecreţia catecholamine

3. Hipersecreţia insulin

58. (1.3) what causeshypoglycemia?
6. 1. Hiposecreţia glucocorticoizilor
59. (1.3) what causeshypoglycemia?
6. 1. renal Glucozuria
15. Hiperseceţia insulin
hipersecreţia
69. what causes hypoglycemia?
17. 1. Hipersecreţia insulin
19. Hiperseceţia insulin
61. (2) which is one ofeacţiile compensation in hypoglycemia?
3. Hiposecreţia glucagonului
4. intensifying lipogenezei
5. Hiposecreţia glucocorticoizilor.
2. Hiposecreţia glucagonului
3. Hipersecreţia glucagonului
intensifying lipogenezei
Hiposecreţiaglucocorticoizilor.
Hiposecreţia glucagonului
intensifying glicogenolizei
64. (2). That is one ofthe compensatory eacţiile hypoglycemia?
1. hiperseceţia insulin
2. hipersecreţia catecholamine
3. hiposeceţia glucocorticosteroizilor
5. thyroid hormone hipersecreţia
intensifying lipolizei
Hiperecreţiaglucocorticoizilor.
intensifying gluconeogenezei
68. (2,3) Which are reacţiile compensatory hypoglycemia?
3. Hipersecreţia glucagonului
70. (2,3) Which are incountervailing eacţiile in hypoglycemia?
intensifying glicogenolizei
2. hipersecreţia catecholamine
Hiperecreţiaglucocorticoizilor.
73. (2, 3) are reacţiile compensatory hypoglycemia?
74. (3) Which is one of the consequences of hypoglycemia?

1. hiponutriţia striated muscles
2. fat hiponutriţia
3. brain hiponutriţia
4. hiponutriţia liver
5. hiponutriţia the immune system
75. (5) how do I change the lipidemia hypoglycemia?
6. into chylomicrons as with hyperlipidemia
7. Hyperlipidemia with VLDL
8. Hyperlipidemia with cholesterol
9. Hyperlipidemia with HDL
10. Hyperlipidemia with fatty acid neesterificaţi
76. (3) how do I change the contents of lipids and glycogen in the liver in hypoglycemia?
11. increase glycogen, lipids are increasing
12. glycogen, lipids increase decrease
13. glycogen, lipids are increasing
14. glycogen, lipids decrease
15. glycogen, lipids are missing
77. (1) the kind of muscular dystrophy is possible in live in long hypoglycemia?
16. lipid-dystrophy
17. Duchenne with cholesterol
18. protein Duchenne
19. glucidică dystrophy
20. hidropică dystrophy
78. (3) Which is one of the consequences of hyperglycemia offood?

1. Coma hiperglicemică.
2. hyperosmolar coma
3. Obesity
4. Lipoinfiltraţia liver
5. Hipercetonemia.
79. (5) Which is one of the consequences of hyperglycemia offood?
3. Lipoinfiltraţia liver
4. Hipercetonemia.
5. Glucozuria
80. (2,5) What are the consequences of hyperglycemia offood?
6. Obesity
8. Hipercetonemia.
9. Glucozuria
81. (1) Which is one of the consequences of hyperglycemia diabetic?

1. Hyperosmolar Coma
2. Obesity
3. metabolic alkalinization
4. oliguria
5. overloading of hepatocytes with glycogen
1. Obesity
2. glucozuria
4. oliguria

1. Obesity
2. Coma cetodiabetică
4. oliguria

1. Obesity
3. Hipercetonemia
4. oliguria

1. Obesity
3. glicozilarea protein
4. oliguria
86. (2,3) what are the consequences of hyperglycemia diabetic?

1. Obesity
6. Hyperosmolar Coma
8. oliguria
1. Obesity
10. glucozuria
12. oliguria
1. Obesity
14. Coma cetodiabetică
16. oliguria
1. Obesity
18. Hipercetonemia
20. oliguria
90. (3) Which is the cause of galactozemiei?

1. Excessive lactozwith milk.
2. The transformation of glucose Galactose
3. The inability of the liver to convert Galactose into glucose
4. The inability of authorities to transform the Galactose into glucose
5. Inability of the kidneys to excrete Galactose
91. (4) Which is the cause of galactozemiei?
8. The inability of transform Galactose into glucose
9. The inability of police to use galactose.
10. The inability of the kidney to secrete Galactose
92. (4.5) Which are the causes of galactozemiei?
13. The inability of transform Galactose into glucose
14. The inability of police to use galactose.
15. The inability of the liver to convert Galactose into glucose
93. (5) which is one of the consequences of galactozemiei to newborn babies?

1. Coma hipergofitactozemică.
2. galactozuria
3. Diabetes mellitus.
4. obesity
5. The infiltration of the galactose.
1. galactozuria
3. obesity
4. Opacificarea lens.
2. galactozuria
4. obesity
5. Dismorfogeneza nevros central system.
96 (5) which is one of the consequences of galactozemiei to newborn babies?
6. galactozuria
8. obesity
9. intoxication with Galactose degradation metabolites
97. (4.5) Which are the consequences of galactozemiei to newborn babies?
10. galactozuria
12. The infiltration of the galactose.

14. galactozuria
16. Opacificarea lens.

18. Dismorfogeneza nevros central system.
20. obesity
100. (2) how do I change compoziuţia to blood drinking foodstuff of lipide?

1. Hyperlipidemia with very low density lipoprotein
2. Into chylomicrons as with Hyperlipidemia
3. Hyperlipidemia with fatty acid neesterificaţi
4. Hyperlipidemia with low density lipoprotein
101. (3) Which is one of the consecinţele metabolism of the consumption food excessively
lipide?
1. gluconeogeneza
2. increased lipid catabolism
3. intensifying lipogenezei
4. Cetogeneza
5. lipiduria
102. (3) Which is one of the cmetabolic onsecinţele of consumption excessive lipide?
6. gluconeogeneza
7. increased lipid catabolism
8. obesity
9. Cetogeneza
10. lipiduria
103. (3) Which is one of the consecinţele inaniţiei lipid?

1. Unbalanced energy Deficit
2. Saturated fatty acids Deficiency
3. Fat-soluble vitamins Deficiency.
4. HDL deficiency
5. lack of glycerol
104. (3) Which is one of the consecinţele inaniţiei lipid?
3. Polyunsaturated fatty acids Deficiency
4. HDL deficiency
5. lack of glycerol
105. (3.5) Which are consecinţele inaniţiei lipid?

8. Polyunsaturated fatty acids Deficiency
9. HDL deficiency
10. Fat-soluble vitamins Deficiency.
106. (4) Which is one of the cauzele maldigesiei lipids?

1. Hiposecreţia salivary lipase
2. Hiposecreţia gastric fosfolipazei
3. hiposecreţia gastric lipase
4. Hiposecreţia pancreatic lipase
5. Hiposecreţia intestinal lipase
107. (4) Which is one of the cauzele maldigesiei lipids?
6. Hiposecreţia salivary
7. Gastric Hipoaciditatea
8. hiposecreţia gastric lipase
9. Hiposecreţia ball
10. Small bowel mucosa Lesions
108. (3.4) Which are cauzele maldigesiei lipids?
11. Hiposecreţia salivary
12. Gastric Hipoaciditatea
13. Hiposecreţia salivary lipase
15. Small bowel mucosa Lesions
109. (5) Which is one of the consecinţele maldigestiei lipids?

1. unbalanced energy deficit
2. Phospholipid deficiency
3. cholesterol deficiency
4. lipogenezei malfunction
5. polyunsaturated fatty acids deficiency
1. disruption of hormone synthesis steroids
4. Blood Hipocoagulabilitatea
5. Blood Hipercoagulabilitatea
1. lack of fat-soluble vitamins
5. Disturbance hormone synthesis steroids
112. (1,4) Which are consecinţele maldigestiei lipids?
8. polyunsaturated fatty acids deficiency
113. (1.3) Which are consecinţele maldigestiei lipids?
11. Blood Hipocoagulabilitatea
114 . (1) how do I change the blood lipid fractions in m.aldigestia of lipids?
1. decrease chilomicronilor
2. reduction of very low density lipoprotein
3. lowering low density lipoprotein
4. reduction of high density lipoprotein
5. fatty acid neesterificaţi lessening
115. (1) the lipoproteins are absorbed in lipids transported intestin thin?
1. into chylomicrons as.
2. Very low density lipoprotein
3. Low density lipoprotein
4. High density lipoprotein
5. Free Fatty Acids in association with albumin
116 . (1) In the high-density lipoprotein lipids are transported sintetare analyzed in the
liver?
1. Very low density lipoprotein (pre-beta-lipoprotein).
2. Low density lipoprotein (beta-lipoproteins).
3. High density lipoprotein (Alpha-lipoproteins).
4. into chylomicrons as
5. Free Fatty Acids in association with albumin
117. (5) in the form of raised lipids are transported by weavingyour body fat?
1. Into Chylomicrons As
5. Free fatty acid conjugates of albumin.
118 . (3) In what compounds are transported colesterolul for organ ?

1. Into Chylomicrons As.
2. Cholesterol in conjunction with albumin
5. Cholesterol free.
119 . (3) In what compounds are transported colesterolul for organ ?
1. incorporated into chylomicrons as.
120 . (3,5) In which compounds are transported colesterolul for organ ?
1. incorporated into chylomicrons as.
212 . (4) In which fractions of lipoproteins is transported colesterolul from the organs to the
liver ?
122 . (2) Which is one of the cauzele hiperlipidemiei retention?

1. Inability of the kidneys to excrete lipids
2. reduction of lipoproteinlipazei activity
3. Phospholipid synthesis in liver Failure.
4. lack of insulin and inhibition of lipogenezei in adipose tissue
5. excess glucagon and lipolizei in adipose tissue
1. inapacitatea of the kidneys to excrete lipids
2. apoproteine receptor conformation change
1. inapacitatea of the kidneys to excrete lipids
2. changing the conformation of apolipoproteins lipoprotein
1. the inability of the kidneys to excrete lipids
2. decreasing ability to endoteliocitelor lipopectice
126 . (1.3) Which are cauzele hiperlipidemiei retention?
6. 1. reduction of activity lipoproteinlipazei
3. Insufficient synthesis of apoproteinei C in the liver
6. 1. change the apoproteine receptor conformation
6. 1. change the conformation of apolipoproteins lipoprotein
6. 1. reduction of the capacity of endoteliocitelor lipopectice
2. 1. the insufficiency of apolipoproteins E synthesis in the liver
131 . (1) Which is one of the consecinţele hiperlipidemiei?
1. Lipogeneza in adipose tissue and increased obesity
2. increased cholesterol synthesis and ateromatoza
3. increased synthesis of ketone body and hipercetonemia bodies
4. Enhanced lipid Excretion with urine
5. increase of fatty acids gluconeogenezei
132 . (1) what is the consequence of protein absorption from the digestive tract of native
food?
1. Food allergy.
2. Hiperproteinemia. .
3. Intensifying proteolizei
4. Anaphylactic Shock.
5. Penetration of the liver with heterogeneous proteins
133 . (1) how do I change the protein spectrum of blood in hepatic?

1. Serum albumins synthesis Failure with reduction ratio 6/immunoglobulins.
2. Low serum globulin level with increased synthesis of albumin/immunoglobulins.
3. concomitant decrease of the albumins and serum globulin level
4. hipoglobulinemie with hipoonchie
5. Insufficient synthesis of immunoglobulins with immune deficiency
1. Insufficient increase in serum globulin level synthesis report 6/immunoglobulins.
3. hipoalbuminemie with hipoonchie
4. Insufficiency of blood clotting factors
136. (2,4) how do I change the protein spectrum of blood in hepatic insufficiency?
6. Serum albumins synthesis Failure with reduction ratio 6/immunoglobulins.
137. (2,4) how do I change the protein spectrum of blood in hepatic insufficiency?
10. hipoalbuminemie with hipoonchie
138 . (3) Image disorder of the digestive tract can lead to protein maldigestia?
2. Hiposalivaţia.
3. Pancreatic Hiposecreţia
4. gastric hiperaciditatea
5. lack of intestinal proteazelor
139 . (3) Image disorder of the digestive tract can lead to protein maldigestia?
2. Hiposalivaţia.
3. Gastric Anaciditatea.
140. (4) The functions of the digestive tract disorder can lead to protein maldigestia?
2. Hiposalivaţia.
4. Lack of intestinal carboxipeptidazelor.
141. (2.4) The disorder of the digestive tract can lead to protein maldigestia?
6. Pancreatic Hiposecreţia
142. (2.4) The disorder of the digestive tract can lead to protein maldigestia?
10. Gastric Anaciditatea.
143. (1) how do I change the protein metabolism in maldigestia proteins?

1. lack of essential amino acids
2. amino acid deficiency non
3. excess amino acids are essential in the blood
4. proteoliza in myocardium
5. catabolizarea serum for energy proteinelşor
6. excess amino acids and non- in the blood
11. aminoaciduria

1. negative nitrogen balance
2. positive nitrogen balance
3. Hiperproteinemie
147. (1.2) how do I change the protein metabolism in maldigestia proteins?

7. lack of essential amino acids
8. Hiperproteinemie
12. excess amino acids and non- in the blood
13. Hiperproteinemie
17. aminoaciduria
18. Hiperproteinemie
150. (4) how do I change the digestive processes in the large intestine in protein
maldigestia?
1. hipoosmolartatea the contents of the small intestine
2. the formation of excess carbon dioxide
3. training in excess of lactic acid
4. excess of ammonia in the formation
5. Absorption in the blood of protein molecules
maldigestia?
9. training in excess of hydrogen sulphide
maldigestia?
153. (4.5) how to modify the digestive processes in the large intestine in protein
maldigestia?
20. excess of ammonia in the formation
154. (4.5) how to modify the digestive processes in the large intestine in protein
maldigestia?
25. training in excess of hydrogen sulphide
155. (1) In the pathological process to install hipoproteinemia?

1. Total Inaniţia.
2. Diabetes Insipidus
3. Hemoconcentraţia.
4. acute Glomerulonephritis
5. acute renal failure

1. Proteinuria.
2. Diabetes Insipidus
157. (3) the pathological process to install hipoproteinemia?
1. diabetes insipidus
3. Combustiile grade II-III
3. kidney failure, liver failure
159. (3) the pathological process to install hipoproteinemia?
3. nephrotic syndrome
160. (3.5) the pathological processes to install hipoproteinemia?
9. Total Inaniţia.
161. (3.5 In the pathological processes to install hipoproteinemia?
1. Proteinuria.
162. (3.5) the pathological processes to install hipoproteinemia?
16. Combustiile grade II-III
163. (3.5) the pathological processes see install hipoproteinemia?
20. kidney failure, liver failure
164. (1) The person running hipoproteinemia?

1. Hipoonchia plasma.
2. Reduction of kidney as urolithiasis.
3. hiponutriţia organs
4. reduction of gluconeogenezei amino acids and hypoglycemia
5. energy shortage
165. (2) leads to the hipoproteinemia?

1. reduction of kidney as urolithiasis.
2. Swelling.
5. energy shortage
166. (2) leads to the hipoproteinemia?

2. Poliurtake
5. energy shortage
167. (2,4) leads To hipoproteinemia?
6. Poliurtake
8. Hipoonchia plasma.
9. energy shortage
168. (2,4) leads To hipoproteinemia?

10. Poliurtake
2. Swelling.
12. energy shortage
169. (2) the pathological process to install hiperproteinemia?

1. Hemorrhage
2. dehydration
3. Renal Insufficiency.
5. enhancement of protein synthesis by the liver
170. (2) leads to the hiperproteinemia?

1. Swelling.
2. Dehydration interstitial.
3. Poliuria.
4. protein liver dystrophy
5. alergizarea organismuluzi
171. (3) The person running hiperproteinemia?

1. Edema.
2. Intensifying as urolithiasis renale.
5. alergizarea organismuluzi
172. (3.5) leads To hiperproteinemia?
1. Edema.
6. Intensifying as urolithiasis renale.
9. Dehydration interstitial.
173. (1) The substance is formed in excess to intensify nucleoproteidelor catabolism?

1. uric acid.
2. urea.
3. ammonia
4. carbon dioxide
5. biogenic amines
174. (1) In what circumstances is a negative nitrogen balance?

1. Fever.
2. Healthy children.
3. At thedministrarea of insulin.
4. androsteroizilor administration
5. the gestation
1. The children healthy.
3. the remains
5. the gestation
3. The glucocorticoizilor administration.
5. the gestation
177. (3) under what circumstances meets the negative nitrogen balance?
2. thedministrarea of insulin.
3. In stress
5. the gestation
178. (1.3) In what cases it encounters negative nitrogen balance?

6. 1. fever.
6. In stress
8. the gestation

6. 1. remains in
9. In stress
11. the gestation

6. 1. The Administration of glucocorticoizilor.
12. In stress
14. the gestation
181. (2) In what circumstances is a positive nitrogen balance?

1. fever.
2. Healthy children.
5. obesity

1. fever.
5. obesity

1. fever.
3. androsteroizilor management
5. obesity
184. (4) when the meets positive nitrogen balance?

1. fever.
4. Gestation
5. obesity
185. (1.4) In what circumstances is a positive nitrogen balance?
6. 1. thedministrarea of insulin.
8. Gestation
9. obesity
186. (1.4) In what circumstances is a positive nitrogen balance?
6. 1. the administration of androsteroizilor
12. Gestation
13. obesity
187. (5) leads To excessive dietary intake of protein?

1. Hiperproteinemia.
2. proteunuria
3. food allergy
5. dyspepsia in proteins
188. (3) The leading drinking foodstuff of protein?
1. Hiperproteinemia.
2. proteinuria
3. hiperaminoacidemia
4. food allergy
189. (3) The leading drinking foodstuff of protein?
Hiperproteinemia.
proteunuria
aminoaciduria
food allergy
protein liver dystrophy
190. (3) leads To excessive drinking foodstuff of protein?

1. protein of ficatuluiu dystrophy
2. Hipersecreţia ball.
3. creatorea
4. amilorea
5. steatorea
191. (3.5) to the leading drinking foodstuff of protein?
7. creatorea
8. amilorea
9. dyspepsia in proteins
192. (3.5) To the excessive consumption of protein food?
11. creatorea
12. amilorea
13. hiperaminoacidemia
193. (3.5) To the excessive consumption of protein food?
15. creatorea
16. amilorea
aminoaciduria
194. (1) The substance forms in the intestinaltin thick as a result of putrefaction of
proteins?
1. Methane.
2. Lactic acid.
3. uric acid
4. acetate
5. carbon dioxide
proteins?
1. Indolul.
2. Lactic acid.
3. uric acid
4. acetate
5. carbon 2bioxidul
proteins?
1. hydrogen sulfide.
2. Lactic acid.
3. uric acid
4. acetate
5. carbon dioxide
proteins?
21. Putrescina.
2. Lactic acid.
3. uric acid
4. acetate
5. carbon dioxide
197. (1.5) What substances are formed in intestinaltin thick as a result of putrefaction of
proteins?
21. Putrescina.
6. Lactic acid.
7. uric acid
8. acetate
9. Methane.
proteins?
21. Putrescina.
10. Lactic acid.
11. uric acid
12. acetate
1. Indolul.
proteins?
21. Putrescina.
13. Lactic acid.
14. uric acid
15. acetate
1. hydrogen sulfide.
200. (1) The toxic substances causing intestinal autointoxicaţie?

1. putrefaction of protein products
2. carbohydrate fermentation products
3. lipid peroxidation thus interrupting products
4. ectivităţii vital microbial products
5. microbial antigens
201. (1) The pathological process causes intestinal autointoxicaţie?

6. constipation
7. chronic gastritis
8. Enteritis.
9. diarea
10. ulcerative colitis
1. liver Failure.
3. Enteritis.
4. diarea
1. renal Stagnation.
3. Enteritis.
4. diarea
204. (1.5) The pathological processes causing intestinal autointoxicaţie?
7. Enteritis.
8. diarea
9. constipation
205. (1.5) The pathological processes causing intestinal autointoxicaţie?
11. Enteritis.
12. diarea
1. liver Failure.
11. DISHOMEOSTAZIILE ELECTROLYTIC (93)
1. (2) with hipernatriemia?

1. sodium concentration greater than 180 mecv/l;
3. sodium concentration less than 135 mecv/l;
5. higher sodium concentration of 100 mecv/l.
2. (2) the pathological process meets hipernatriemia?

1. chronic suprarenaliană failure;
2. primary aldosteronismul;
3. gaseous alkalinization;
4. dehydration through diarrhea
5. dehydration by vomiting

2. Cushing's syndrome

3. gaseous acidosis.


5. dehydration through increased sweating

5. dehydration through the lung hyperventilation
8 (2.5) In the pathologic processes meets hipernatriemia?

6. primary aldosteronismul;
14. gaseous acidosis.
11. (2.5) In pathological processes that meets hipernatriemia?
12. (2.5) In pathological processes that meets hipernatriemia?
22. dehydration through increased sweating
13. (4) Which is the cause of hipernatriemiei absolute?

1. redistribution of sodium ions between intra-and extracellular sectors;
2. deshidratărea izoosmolară
3. hipersecreţia of ADH;
4. hipersecreţia of aldosterone
5. hiposecreţia of ADH.
14. (3) Which is causing hrelative ipernatriemiei ?

1. retention of sodium ions in the body;
2. redistribution of sodium ions between intra-and extracellular sectors;
3. dehydration hyperosmolar coma
4. increasing the secretion of ADH
5. increased secretion of aldosterone
15. (4) Which is causing hrelative ipernatriemiei?

retention of sodium ions in the body;
redistribution of sodium ions between intra-and extracellular sectors;
increasing the secretion of ADH
decreasing the secretion of ADH.
increased secretion of aldosterone
16. (1,4) Which causes hrelative ipernatriemiei?
6. dehydration hyperosmolar coma
redistribution of sodium ions between intra-and extracellular sectors;
increasing the secretion of ADH
decreasing the secretion of ADH.
increased secretion of aldosterone
17. (1) the compensation mechanism in absolute hipernatriemia?

2. decreased secretion of ADH
3. increased secretion of parathyroid hormone
4. decreasing the secretion of parathyroid hormone;
5. increased aldosterone secretion;
18. (5) compensating mechanism that is in absolute hipernatriemia?
3. decreasing the secretion of parathyroid hormone;
4. increased aldosterone secretion;
5. decreasing the secretion of aldosterone;
19. (5) compensating mechanism that is in absolute hipernatriemia?
4. decreasing the secretion of ADH;
5. activation of secretion of atrial natriuretică peptide
20. (1.5) the mechanisms compensatroii in absolute hipernatriemia?

6. 1. increasing the secretion of ADH
21. (1.5) the mechanisms compensatroii in absolute hipernatriemia?

6. 1. decreasing the secretion of aldosterone;
22. (4) Which is the consequence of hipernatriemiei for cells?

1. swelling of the cell
2. excessive sodium penetration into cells
3. excessive sodium out of the cell
4. cell exicoza
5. maintaining normal cell volume
23. (1) how do I change the concentration of electrolytes in hiperaprimary ldosteronismul ?

1. hipernatriemie and hypokalemia
2. hipernatriemie and hiperkaliemi(e)
3. hiponatriemie and hypokalemia
4. hiponatriemie and hypokalemia
5. hipernatriemie and normokaliemie
24. (3) Which is in hipera oedema of pathogenesis ofprimary ldosteronismul ?

high blood pressure
increased permeability of vessels
excessive accumulation of sodium in the interstice
its edema cells
hipersecreţia Renin
25. (3) the pathological process meets secondary hiperaldosteronismului ?
1. adenomaul glomerulere area of corticosuprarenalelor;

3. heart failure;
4. nephrotic syndrome;
5. Addisson disease
26 (5) In which the pathological process meets the secondary hiperaldosteronismului

?
4. Addisson disease
5. hipovolemia
27 (5) In which the pathological process meets the secondary hiperaldosteronismului ?
4. Addisson disease
5. liver cirrhosis;
28 (5) In which the pathological process meets the secondary hiperaldosteronismului ?
4. Addisson disease
5. renal artery stenosis.
29 (2.5) In the pathologic processes meets the secondary hiperaldosteronismului ?
6. heart failure;
8. Addisson disease
10. hipovolemia
12. Addisson disease
14. liver cirrhosis;

16. Addisson disease
32. (2) the concentration of Na hyponatriemia associated start?

1. 135 mecv/l;
2. 120 mecv/l;
3. 100 mecv/l;
4. 10 mecv/l
5. 5 mecv/l;.
33. (5) what is the cause of absolute hiponatriemiei?

1. increased secretion of АДH;
2. excessive ingestion of liquids hipoosmolare
3. excessive ingestion of glucose solution 5%
4. poliuria in diabetes mellitus
5. insuficent consumption of salt pans
34. (5) what is the cause of absolute hiponatriemiei?

1. hipersecreţia of АДH;
3. excessive ingestion of glucose solution 5%
35. (3.5) Which causes the absolute hiponatriemiei?
7. insuficent consumption of salt pans
36. (1) what is the cause of the relative hiponatriemiei?

3. the synthesis of biologically inactive Renin.
4. total suprarenaliană insufficiency
5. gaseous alkalinization
37. (1) what is the cause of the relative hiponatriemiei?

4. total suprarenaliană insufficiency
38. (1.4) That causes hiponatriemiei drift?
39 (4) that the hormone participates in maintaining homeostasis of potassium in the body?
tireocalcitonina
parathormonul
thyroxine.
aldosterone
natriuretic hormone
40. (3) The minimum value of the concentration of potassium indicate

hyperkalemia?
3.5 mecv/l;
5 mecv/l
5.5mecv/l;
7mecv/l;
10mecv/l;
41. (1) In the pathological process meets absolute hyperkalemia?

Renal insficienţa;
hipersecreţia of aldosterone
hipersecreţia of parathyroid hormone
hipersecreţia of tireocalcitonină
hipersecreţia of antidiuretic hormone

1. deep tissue protein catabolism

1. hipoaldosteronism
44. (2) the pathological process meets absolute hyperkalemia?

secreţei reduction of Renin
45. (5) the pathological process meets absolute hyperkalemia?
massive hemolysis
46. (2, 5) In the pathologic processes meets absolute hyperkalemia?
Renal insficienţa;
massive hemolysis
47. (2,5) the pathological processes is absolute hyperkalemia?

1. deep tissue protein catabolism
massive hemolysis

1. hipoaldosteronism
massive hemolysis

secreţei reduction of Renin
massive hemolysis
50. (2) how do I change the cardiovascular functions hyperkalaemia?

tachycardia;
bradicardie;
hypertension
atrioventricular block
cardiac arrest in systole.
51. (5) how do I change the cardiovascular functions hyperkalaemia?

Sinus tachycardia;
tachycardiaparoxysmal
hypertension
atrioventricular block
the cardiac diastole.
52. (4.5) how do I change the cardiovascular functions hyperkalaemia?
Sinus tachycardia;
tachycardiaparoxysmal
hypertension
bradicardie;
the cardiac diastole.
53. (2) The minimum value of the concentration of potassium indicates hipokaliemie?
2.5mecv/l
3, 5mecv/l;
5 mecv/l;
7 mecv/l;
10 mecv/l;
54. (1) the cause hipokaliemiei?

treatment with glucocorticoids;
total suprarenaliană insufficiency
matabolică acidosis;
Diabetes Insipidus.
intense hemolysis
55. (1) the cause hipokaliemiei?

1. treatment with insulin;
total suprarenaliană insufficiency
Diabetes Insipidus.
intense hemolysis
56. (5) hipokaliemiei what is the cause?
1. total failure suprarenaliană
Diabetes Insipidus.
intense hemolysis
hyperaldosteronism
57. (2.5) That causes hipokaliemiei?
treatment with glucocorticoids;
Diabetes Insipidus.
intense hemolysis
hyperaldosteronism
58. (2.5) That causes hipokaliemiei?

1. treatment with insulin;
Diabetes Insipidus.
intense hemolysis
hyperaldosteronism
59 (4) Which is the mechanism of pathogenesis in chronic liver afecţiunele hipokaliemiei?

1. disruption of protein synthesis;
2. disruption of Glycolysis;
glicogenolizei disorders;
aldosteronului degradation disorders
derglarea glucocorticoizilor degradation
60. (1) by the parathormonul mechanism regulates calcium homeostasis?

contribute to calcium absorption from the gastrointestinal tract;
intensifying processes of osteosynthesis;
intensifying removal of calcium salts in bile;
It stimulates the secretion of calcium through the renal distal miniscule tubules;
decreases the reabsorption of calcium renal proximali in miniscule tubules.
61. (2) Through the parathormonul mechanism regulates calcium homeostasis?
1. reduces calcium absorption from the gastrointestinal tract;
intensified osteoliză processes and release of calcium;
decreases the reabsorption of calcium renal proximali in miniscule tubules.
62. (5) Through the parathormonul mechanism regulates calcium homeostasis?
stimulates renal calcium reabsorption in the miniscule tubules proximali.
63. (3.5) Through what mechanisms regulate Calcium Homeostasis parathormonul?
contribute to calcium absorption from the gastrointestinal tract;
64. (3.5) Through what mechanisms regulate Calcium Homeostasis parathormonul?
intensified osteoliză processes and release of calcium;
65. (1) by the tireocalcitonina mechanism regulates calcium homeostasis?

osteoliza and release calcium intensifies;
active secretion of calcium intensifies through the renal distal miniscule tubules;
66. (2) Through the tireocalcitonina mechanism regulates calcium homeostasis?
1. stimulates calcium absorption from the gastrointestinal tract;

osteosynthesis and intensifies the incorporation of calcium;
67. (5) Through the tireocalcitonina mechanism regulates calcium homeostasis?

inhibits the reabsorption of calcium renal proximali in miniscule tubules.
68. (3.5) Through what mechanisms regulate Calcium Homeostasis tireocalcitonina?

69. (3.5) Through what mechanisms regulate Calcium Homeostasis tireocalcitonina?

osteosynthesis and intensifies the incorporation of calcium;
70. (3) Ec grievous complcaţie causing hypocalcemia in children?

acute renal failure;
hipoosmolară coma;
spazmofilia;
suprarenaliană acute failure;
myasthenia
71. (4) Ec grievous complcaţie causing hypocalcemia in children?
1. acute renal failure;
hipoosmolară coma;
tonic seizures and smother.
myasthenia
72. (1.4) serious hypocalcemia causing complcaţie in children?
1. spazmofilia;
hipoosmolară coma;
tonic seizures and smother.
myasthenia
73. (1) what is the cause of secondary hipercalcemiei?

excessive intake of calcium in the body;
renal fosfatdiabetul
Hypovitaminosis D
metabolic alkalinization;
hiperscreţia mineralocorticosteroizilor
74. (2) That is causing the side hipercalcemiei?
hipervitaminoza D;
Hypovitaminosis D
75. (4) That is causing the side hipercalcemiei?
Hypovitaminosis D
metabolic acidosis;
76. (1,4) Which causes secondary hipercalcemiei?
Hypovitaminosis D
metabolic acidosis;
77. (1,4) Which causes secondary hipercalcemiei?

Hypovitaminosis D
metabolic acidosis;
78. (1) the pathogenesis mechanism of the hipercalciemiei?

increased resorption of bone tissue;
reduction of bone tissue resorption;
increasing renal excretion;
metabolic acidosis
chronic renal insufficiency
79. (1) the pathogenesis mechanism of the hipercalciemiei?
increased absorption in the intestine As;
metabolic acidosis
chronic renal insufficiency
80. (1.5) Which are the hipercalciemiei pathogenetic mechanisms?
increased absorption in the intestine As;
metabolic acidosis
81. (1) the cause hipocalcemiei?

hipofuncţia parathyroid glands
hiperfuncţia parathyroid glands
hipersecreţia tireocalcitoninei
hipersecreţia natreiuretic hormone
speeding Renin

Renal insuficienşa;
speeding Renin
reduction of bone tissue sensitivity to parathyroid hormone.
speeding Renin
84. (1.3) That causes hipocalcemiei?
hipofuncţia parathyroid glands
speeding Renin
85. (1.3) That causes hipocalcemiei?
Renal insuficienşa;
speeding Renin
86. (1) the pathogenesis mechanism of the hipocalciemiei?
osteoblaştilor stimulation
increasing calcium renal secreţei in miniscule tubules;
alcaloze calcium depletion
hyperparathyroidism
reduction of calcium absorption in the small intestine
hyperparathyroidism
increased calcium excretion by the kidneys;
hyperparathyroidism
hyperparathyroidism
90. (1,4) Which are the hipocalciemiei pathogenetic mechanisms?
osteoblaştilor stimulation
hyperparathyroidism
reduction of calcium absorption in the small intestine
hyperparathyroidism
increased calcium excretion by the kidneys;
hyperparathyroidism
93. (5) Which is the limitation of hipocalciemiei mechanism of bile in the intestine?
lack of cholesterol in the intestine
decrease in the synthesis of vitamin D;
decrease the absorption of vitamin D
disorders of vitamin D processing in active form
saponification of lipids with As in the gut;
12. PATHOPHYSIOLOGY of ACID/BASE (61)
1. (1) the accumulation of endogenous substances which may lead to acidosis?

ketone body substances
acetic acid
pyruvic acid
uric acid
oxalacetic acid
CO2
acetic acid
pyruvic acid
uric acid
oxalacetic acid
lactic acid
acetic acid
pyruvic acid
uric acid
oxalacetic acid
4. (1.5) the accumulation of endogenous substances which may lead to acidosis?

lactic acid
acetic acid
pyruvic acid
uric acid
ketone body substances
5. (1.5) the accumulation of endogenous substances which may lead to acidosis?

lactic acid
acetic acid
pyruvic acid
uric acid
CO2
6. (1) Which is criteriul acidozher ?

1. decreasing the pH.
2. increasing the pH.
4. reduction of the concentration of H+
6. alkaline reserve Accumulation
7. acidification of the urine
2. Increase the concentration of the ions H+.
3. reduction of the concentration of H+
4. accumulation of alkaline reserve

2. decreasing the concentration of H+
3. alkaline reserves
9. (3.5) what are the criteria acidozthey ?

5.1. Decreasing the pH.
10. (3.5) what are the criteria acidozthey ?
5.2. Increasing the concentration of the ions H+.
11. (2) Which is criteriul tolcalozher ?

3. increasing the concentration of hydrogen ions
4. Reducing alkaline reserve
5. urinary alkalinization of urine

2. decreasing the concentration of H +.
3. increasing the concentration of hydrogen ions

2. increase of the concentration of hydrogen ions
3. excess reserve Accumulation alkaline
14. (3,4) what are the criteria oflcalozthey ?
4. 2. Increasing the pH.
15. (3,4) what are the criteria oflcalozthey ?

4. 2. Decreasing the concentration of H +.
16. (3) What we call compensated acidosis?

Decreasing decreasing pH alkaline reserve.
Decrease with increasing pH value alkaline reserve.
Alkaline pH reserves decrease steadily
Alkaline pH reserves increase steadily.
5. constant alkaline Reserveconstant, pH
17. (1) what is known as Decompensated acidosis?

1. reduction of alkaline pH decrease reserves.
2. Decrease with increasing pH value alkaline reserve.
3. Alkaline pH reserves decrease steadily
4. increase the alkaline pH reserves constant.
18. (4) What we call compensated alkalosis?
4. increase the alkaline pH reserves constant.
19. (4) what is known as Decompensated alkalosis?

4. increase the alkaline pH reserves increased
20. (2) the process of respiratory acidosis occurs?

1. pulmonary Hiperventilaţia
2. pulmonary Hipoventilaţia
4. atmospheric hipobaria
5. Alpine sickness
6. caisson disease
21. (2) the process of respiratory acidosis occurs?
1. pulmonary Hiperentilaţia
2. disruption of gas diffusion in alveoli-capillary
4. Alpine sickness
5. caisson disease
22. (2.4) In respiratory acidosis occurs what processes?
1. pulmonary Hiperentilaţia
2. disruption of gas diffusion in alveoli-capillary
4.2. Pulmonary Hipoventilaţia
5. caisson disease
23. (3) the metabolic acidosis occurs process?

1. inaniţia protein
2. inaniţia lipid
3. cetogeneza
4. stepping up proteolizei
24. (3) the metabolic acidosis occurs process?
2. inaniţia lipid
4. stepping up proteolizei
25. (3,4) In metabolic acidosis occurs what processes?

2. inaniţia lipid
4.3. cetogeneza
26. (2) In what process occurs excretory acidosis?

1. Poliuria in Diabetes Insipidus
2. hipersalivaţia with loss of saliva
4. frequent vomiting
5. the abundant perspiration
28 (4) what process occurs in the excretory acidosis?
4. profuse diarea
5. the abundant perspiration
29. (4,5) In which acidosis occurs excretory processes?

4. profuse diarea
5.2. hipersalivaţia with loss of saliva
30. (2) Which ispathogenetic to actorl excretorii acidosis?

1. excessive Formation of CO2.
2. loss of bicarbonates with saliva in the hipersalivaţie
3. excessive CO2 Loss in alveolar hiperventilaţia.
4. loss of bicarbonates with gastric juice in vomiting
5. loss of bicarbonates in the sweat sweating
31. (2) Which ispathogenetic to actorit metabolic acidosis?
2. Excessive formation of lactic acid.
32. (2) Which ispathogenetic to actorit metabolic acidosis?
2. excessive Formation of ketone body bodies.
33. (2,5) What are the factors of patogeneticiit excretorii and metabolic acidosis?
5.2. Loss of bicarbonates with saliva in the hipersalivaţie
34. (2.5) Which are fpatogenetici of actorsit metabolic acidosis and excretorii?
5. 2. Excessive formation of lactic acid.
35. (3) Which ispathogenetic to actorit alcalozelor?

1. Insufficient formation of ketone body bodies.
2. abundant Excretion of uric acid
3. disturbance on the synthesis of urea from ammonia.
4. profuse diarrhea
5. poliuria
2. excessive Ingestion of bicarbonates
4. profuse diarrhea
5. poliuria
3. loss of hydrochloric acid gastric juice.
4. profuse diarrhea
5. poliuria
4. profuse diarrhea
5. poliuria
39. (1,3) patogenetici factors of alcalozelor?
1. 3. disturbance on the synthesis of urea from ammonia.
4. profuse diarrhea
5. poliuria
1. 2. excessive Ingestion of bicarbonates
4. profuse diarrhea
5. poliuria
1. 3. loss of hydrochloric acid gastric juice.
4. profuse diarrhea
5. poliuria
42. (1) Which is reacţia compensatory renal acidosis in?

HCO3 reabsorption of ions in hydrogen ion exchange
Poliuria
Oliguria
carbonic acid removal
retain root hidroxilOH-
43 . (1) what is the reacţia compensatory renal acidosis in?
Renal excretion of H + ions (acidogeneză)
2. Poliuria
3. a iguria
4. Elimination of carbonic acid
5. hold the square root hidroxilOH-
Renal reabsorption of Na + ions in hydrogen ion exchange
Poliuria
Oliguria
Synthesis and elimination of renal ion NH4 (amoniogeneza).
Poliuria
Oliguria
46. (1.3) Which are reacţiile compensatory renal acidosis in?
Poliuria
HCO3 reabsorption of ions in hydrogen ion exchange
Poliuria
Renal excretion of H + ions (acidogeneză)
Renal reabsorption of Na + ions in hydrogen ion exchange
Oliguria
49. (1) Which is reacţia compensatory respiratory acidosis in?

Alveolar Hiperventilaţia.
alveolar hipoventilaţia
increase lung perfusion
Kitaev reflex
arteriovenous pulmonary circuit bridging
50. (5) Which is the consequence of acidosis?
1. incorporation of The plasmatic qn bones.
2. hipoventilaţie flveolară
3. high blood pressure
4. hipocalciemie
1. Incorporation As qn bones.
2. respiratory Acidosis
Hipertensine pressure
hipocalciemie
the removal of bone and osteoporosis
2. alveolar hipoventilaţie
Hipertensine pressure
hipocalciemie
hipercalciemie
53. (3.5) Which are the consequences of acidosis?
hipocalciemie
hipercalciemie
54. (3.5) Which are the consequences of acidosis?
the removal of bone and osteoporosis
hipocalciemie
hipercalciemie
55. (1) Which is rcountervailing eacţia in alcaloze?

1. renal reabsorption of ions (H)+.
2. Synthesis and elimination of renal ion NH4.
3. Ion Reabsorption of HCO3-
4. excessive removal of ammonium
5. hipercalciemie
56. (1) Which is rcountervailing eacţia in alcaloze?
1. removal of the renal Na + ions.
3. Ion HCO3 Reabsorption-
5. hipercalciemie
57. (2) r isa countervailing eacţia in alcaloze?

2. renal excretion of HCO3-ions-.
5. hipercalciemie
58. (2) r isa countervailing eacţia in alcaloze?

2. incorporation As in bones.
5. hipercalciemie
59. (2.4) are reacţiile alcaloze compensatory?

4. 1. Renal reabsorption of ions H+.
5. hipercalciemie
60. (2,4) Which are reacţiile alcaloze compensatory?
4. 1. Renal elimination of Na + ions.
5. hipercalciemie
61. (2,4) Which are reacţiile alcaloze compensatory?
4. 1. Renal elimination of Na + ions.
5. hipercalciemie
12. DIZOXIILE (64)

2. What is known as hypoxia?
reduction of the oxygen content in the blood.
decreasing the content of oxygen in the tissues.
the oxygenation of the blood disorder in the lungs
reduction of partial pressure of oxygen in the air.
5. reduction of the oxygen content in cells
(2)
3 . What we call obstruction?

reduction of the oxygen content in the blood.
decreasing the content of oxygen in the tissues.
the oxygenation of the blood disorder in the lungs
reduction of partial pressure of oxygen in the air.
5. reduction of the oxygen content in cells
(1)
4. (1) the vulnerability of various organs depends to hypoxia?
Biological oxidative processes yield ak

the ability of various structures to fix oxygen
reserves of oxygen in the body
dissociation of oxihemoglobinei ability in organ
the degree of hypoxia
the ability of the body to generate energy on anaerobic pathway

the ability of various structures to fix oxygen
dissociation of oxihemoglobinei ability
the intensity of the oxygen consumption by the body

the ability of various structures to fix oxygen d e
7. (1.5) Of the various vulnerability depends on the organ towards hypoxia?

Biological oxidative processes yield ak
8. (1.5) Of the various vulnerability depends on the organ towards hypoxia?

the ability of the body to generate energy on anaerobic pathway
9. (2) what is the vulnerability of various organs to hypoxia (in descrescândă order)?
brain-muscles smooth-kidney-liver-skin
brain-kidney-liver-smooth muscles-skin
brain-muscles smooth-skin-liver-kidney-
striated muscles-brain-kidney-liver-skin
brain-muscles-muscles striated, smooth muscle-liver-skin
10. what type of hypoxia develops in Alpine disease?

exogenous normobarică
exogenous hyperbaric
exogenous hipobarică
respirator
histotoxică
(c)
11. what type of hypoxia develops in disorders of intracellular processes use oxygen?
histotoxică
cardiogenă
respirator
Interstitial
rose
(a)
12. (1) the pathogenesis of hypoxia with nitrite poisoning in hemice?

1. decreasing affinity for oxygen of methemoglobinei
2. decreasing affinity for oxygen of caboxihemoglobinei
3. decreasing affinity for oxygen of carbhemoglobinei
4. decreasing affinity for oxygen of hemoglobin with 4 beta chains
5. decreasing the affinity of hemoglobin for oxygen with 4 Alpha chains
13. (4) Which is hemice in the pathogenesis of hypoxia hemoglobinopatii?

4. decreasing affinity for oxygen of hemoglobin with 4 beta chains
5. decreasing the affinity of hemoglobin for oxygen with bivalent iron
14. (4) Which is hemice in the pathogenesis of hypoxia hemoglobinopatii?
15. (4.5) Which is hemice in the pathogenesis of hypoxia hemoglobinopatii?
5.4. decreasing the affinity of hemoglobin for oxygen with 4 beta chains
16. (4) Which is hemice hypoxia in the pathogenesis of hemorrhage?
4. reduction of the absolute capacity of the blood oxigenice
17. (2) Which is hemice hypoxia in the pathogenesis of poisoning with carbon monoxide?
6. reduction of the absolute capacity of the blood oxigenice
7. decrease in the affinity of hemoglobin for oxygen with bivalent iron
18. (1) the histotoxică hypoxia develops?

cyanide poisoning
CO poisoning
poisoning with a2
nitrate poisoning
acetic acid poisoning
respiratory chain enzymes synthesis disorder
CO poisoning
poisoning with a2
nitrate poisoning
thyrotoxicosis
CO poisoning
poisoning with a2
nitrate poisoning
alteration of mitochondria
CO poisoning
poisoning with a2
nitrate poisoning
22. (1.3) In the State of hypoxia develops histotoxică?
CO poisoning
cyanide poisoning
nitrate poisoning
CO poisoning
respiratory chain enzymes synthesis disorder
nitrate poisoning
CO poisoning
thyrotoxicosis
nitrate poisoning
25. (1) the State of dissociation curve deviate to the right oxihemoglobinei?
acidosis
alkalosis
hipocapnie
hypothermia
suplusul of hemoglobin in erythrocytes
1. alkalosis
2. hipocapnie
3. hypercapnia
4. hypothermia
5. suplusul of hemoglobnă in red cells
1. alkalosis
2. hipocapnie
3. hyperthermia
4. hypothermia
5. suplusul of hemoglobnă in red cells
28. (3.5) In what state of dissociation curve deviate to the right oxihemoglobinei?
1. alkalosis
2. hipocapnie
3. hyperthermia
4. hypothermia
5. acidosis
29. (3.5) In what state of dissociation curve deviate to the right oxihemoglobinei?
1. alkalosis
2. hipocapnie
3. hyperthermia
4. hypothermia
5. 3. hypercapnia
30. (2) the State of dissociation curve deviate to the left oxihemoglobinei?
acidosis
alkalosis
hypercapnia
hyperthermia
surlusul of the erythrocyte hemoglobin
1. acidosis
2. hypercapnia
3. hipocapnie
4. hyperthermia
5. surlusul hemoglobin in erythrocyte
1. acidosis
2. hypercapnia
3. hyperthermia
4. hypothermia
5. surlusul hemoglobin in erythrocyte
33. (4.5) In the pathologic dissociation curve deviate to the left oxihemoglobinei?
1. acidosis
2. hypercapnia
3. hyperthermia
4. hypothermia
5. alkalosis
34. (4.5) In the pathologic dissociation curve deviate to the left oxihemoglobinei?
1. acidosis
2. hypercapnia
3. hyperthermia
4. hypothermia
5. hipocapnie 3.
35. (1) by what is brain hypoxia?

headache
neurosis
chills
psychosis
sustainable excitation
euphoria
neurosis
chills
psychosis
excitation
inappropriate behavior
neurosis
chills
psychosis
38. (1.4) Through what is brain hypoxia?
neurosis
chills
headache
39. (1.4) Through what is brain hypoxia?
neurosis
chills
euphoria
40. what pathological processes in the brain develops at low partial pressure of O2 in
arterial blood below 20 mmHg?
cerebral coma
headache
vertije
obnubilare
drowsiness
(a)
41. What is exacerbation "?

partial pressure of O2 increased in tissues as a result of excessive intake of O2
partial pressure of O2 increased in tissues as a result of its consumption decrease
increasing the pressure of O2 in the blood as a result of the intensification of arterializării
blood plamânilor
partial pressure of O2 increased in tissues as a result of intensifying systemic blood
circulation
increased pressure O2 in tissues as a result of excessive intake of O2 or its consumption
decrease
(e)
42. under what conditions increases the rate of a2 dissolved in the blood?
hiperoxie + normobarie
hiperoxie + hipobarie
hiperoxie + hiperbarie
alveolar hiperventilaţia in normobarie
alveolar hiperventilaţia in hipobarie
(c)
43. (3) the process develops exacerbation "hiperdinamică?
systemic arterial hipertensine
tachycardia
increasing blood flow to the organs
Isometric heart hiperfuncţie
hiperfuncţie heterometrică heart
44. (3) Through what is often hypoxic and hiperdinamică?

increased concentration of Hb (2)4 in arterial blood more than 96%
increasing the amount of oxygen dissolved in the blood plasma
venous blood with arterializarea lessening the arteriovenous difference of O2
conentraţiei reduction of CO2 in venous blood
arteriovenous difference in growth of a2
45. (1) the Image is often hypoxic and dismetabolică?
the excess of oxygen in tissue as a result of its use to a disorder adequate intake
excsiv intake of oxygen into the tissue that exceeds current needs
the excess of oxygen in tissue as a result of anaerobic processes signify upon the oxidative
the excess of oxygen in tissue as a result of intensified catabolic processes
the excess of oxygen in tissue as a result of a reduction in anabolic processes
46. (5) what is often hypoxic and dismetabolică?
1. excsiv intake of oxygen into the tissue that exceeds current needs
2. the excess of oxygen in tissue as a result of anaerobic processes signify upon the oxidative
3. excess of oxygen in tissue as a result of intensified catabolic processes
4. the excess oxygen in tissue as a result of a reduction in anabolic processes
5. excess of oxygen in tissue as a result of inhibition of the respiratory chain enzyme activity
47. (1.5) that is often hypoxic and dismetabolică?
1. the excess of oxygen in tissue as a result of its use to a disorder adequate intake
2. the excess of oxygen in tissue as a result of anaerobic processes signify upon the oxidative
3. excess of oxygen in tissue as a result of intensified catabolic processes
4. the excess oxygen in tissue as a result of a reduction in anabolic processes
5. excess of oxygen in tissue as a result of inhibition of the respiratory chain enzyme activity
48. what applies pressure oxygen for medical purposes?

2-3 ata
4-5 ata
5-7 ata
7-8 ata
10-12 thread
(a)
49. What is contraindicated pathology therapeutic application of oxygen?

chronic diseases of the respiratory system
chronic cardiovascular diseases
bleeding
anemia
tumor processes
(e)
50. (1) what is the harmful effect of hiperoxiei?

lipid cell membrane phospholipids
enhancement of oxidation in the mitochondria and depletion of nutrient substrates
increasing the amount of ATP in the cell
the Krebs cycle activity picks up
pulmonary hipoventilaţia with respiratory acidosis

1. lipid protein
2. enhancement of oxidation in the mitochondria and depletion of nutrient substrates
3. increasing the amount of ATP in the cell
5. respiratory acidosis with pulmonary hipoventilaţia
1. lipid DNA and RNA
2. enhancement of oxidation and depletion of nutrient substrates
increasing the amount of ATP in the cell
pulmonary hipoventilaţia with respiratory acidosis
1. increased concentration of oxihemoglobină in red cells

2. increased concentration of carbohemoglobină in red cells
decreased concentration of carboxiemoglobină in red cells
decreased concentration of dissolved carbon dioxide in the blood
increased concentration of dissolved nitrogen in the blood

2. increased concentration of carboxiemoglobină in red cells
increased concentration of dissolved oxygen in the blood

2. increased concentration of carboxiemoglobină in red cells
increased concentration of carbon dioxide dissolved in the blood

2. metabolic alkalosis
3. respiratory alkalosis
4. respiratory acidosis
5. metabolic acidosis respiratory alkalosis +
57. (1.4) Which are the harmful effects of hiperoxiei?
4. lipid cell membrane phospholipids
58. (4) what are the harmful effects of hiperoxiei?
4. 1. lipid protein
59. (1,4) Which are the harmful effects of hiperoxiei?
4. 1. lipid DNA and RNA
4. 2nd carbohemoglobină in increased concentration of red blood cells
4. increased concentration of dissolved oxygen in the blood
62. (1.4) Which are the harmful effects of hiperoxiei?
4. increased concentration of carbon dioxide dissolved in the blood
63. (3) Which is the accumulation of CO2 in hiperoxie?
1. decreasing the affinity of hemoglobin for CO2

2. the competition CO and CO2 for Hb
Hb saturation with O2
Hb saturation with CO2
increasing the solubility of CO2
64. How do I change hiperoxie in NEONATAL?
respiratory alkalosis
respiratory acidosis
metabolic acidosis
metabolic alkalosis
metabolic acidosis + brespiratorie alkalinization
(2)
14. the SHOCK. Terminal States (88)

1 . (5)That is the main pathogenetic link shock of any etiology?
generalized hypoxia
General hiponutriţia
General hipoenergogeneza
generalized metabolic acidosis
General hipoperfuzia
3. (1) how do I change the activity in the CNS compensated shock?

simpato-adrenal system
inhibition of simpato-adrenal system
activation of the parasympathetic autonomic nervous system
inhibition of the parasympathetic autonomic nervous system
Nice and prasimpatică nuroplegie
4. (4) how do I change the shock offset endocrine activity?
2. hiposecreţia glucocorticosteroizilor
hiposecreţia ADH
hipersecreţia of Renin
hiposecreţia of Renin

1. hiposecreţia of Catecholamines
hiposecreţia ADH
hipersecreţia natriuretic hormone

1. hipersecreţia of Catecholamines
hiposecreţia glucocorticosteroizilor
hiposecreţia ADH
7. (2) how to change produce endocrine activity levels in compensated shock?
hiposecreţia glucocorticosteroizilor
hiposecreţia ADH
hipersecreţia ADH
hiposecreţia ADH

2. hiposecreţia of aldosterone
gonadoliberinelor-gonadotropinelor hipersecreţia-sexuaţi hormone
hiposecreţia Renin
the scarcity of angiotensin
2. hipersecreţia sexuaţi hormones
hiposecreţia sexuaţi hormones
hiposecreţia Renin
11. (2,4) how to change produce endocrine activity in compensated shock?
2. hipersecreţia of Renin
hiposecreţia Renin
hipersecreţia sexuaţi hormones
12. (2, 3) on how to change produce endocrine activity in compensated shock?
hiposecreţia Renin
13. (2.3) how do I change the shock offset endocrine activity?
2. 1. hipersecreţia of Catecholamines
hiposecreţia Renin
2. 2. hipersecreţia glucocorticoizilor
hiposecreţia Renin
2. hipersecreţia ADH
hiposecreţia Renin
2. hipersecreţia ADH
hiposecreţia Renin
17. (2) how to change the shocks to compensate cardiovascular functions?

generalized spasm of microvaselor
vessel spasm with alpha-adrenoceptors
vessel spasm with beta-adrenoceptors
bradycardia
pulmonary hypertension
1. generalized spasm of microvaselor
2. dilating with beta-adrenoceptors
hypertension in high
bradycardia
2. cardiotrope positive effects
cardiotrope adverse effects
hypertension in high
20. (4) how do I change the shock offset cardiovascular functions?
2. great circuit high
bradycardia
paroxysmal
21. (4.5) on how to change the shocks to compensate cardiovascular functions?
bradycardia
paroxysmal
vessel spasm with alpha-adrenoceptors
bradycardia
paroxysmal
2. dilating with beta-adrenoceptors
bradycardia
paroxysmal
2. cardiotrope positive effects
24. (1) The pathological processes it develops in the kidney in compensated shock?
Kidney ischemia
venous hyperemia of the kidney
Kidney hiperperfuzia
poliuria
hipostenuria
25. (2) The pathological processes it develops in the kidney in compensated shock?
1. venous hyperemia of the kidney
2. kidney hipoperfuzia
poliuria
hipostenuria
26. (1.2) The pathological processes it develops in the kidney in compensated shock?
1. kidney ischemia
2. kidney hipoperfuzia
poliuria
hipostenuria
27. (1) Cuzm changes the Renin-angiotensine-aldoasteron in compensated shock?

1. increase the secretion of Renin-Angiotensin II increases aldosterone increases
2. increase the secretion of Renin-angiotensin I to increase increase aldosterone
3. Renin secretion decreases, increases Angiotensin II, aldosterone and increases
4. increase the secretion of Renin-Angiotensin II increases decreases aldosterone
5. increase the secretion of Renin-angiotensin I to increase decreases aldosterone
28. (2) how do I change filtraţia canaliculară reabsorption and Glomerular in compensated
shock?
1. filtaţia increase; increase water reabsorption; reabsorption increase muscle function
2. filtaţia falls; increase water reabsorption; reabsorption increase muscle function
3. filtaţia falls; reabsorption of water drops; muscle function decreases the reabsorption
4. filtaţia increase; reabsorption of water drops; reabsorption increase muscle function
5. filtaţia increase; increase water reabsorption; muscle function decreases the reabsorption
29. (2) how do I change the shock diuresis compensated?

1. polyuria
2. oliguria
3. hipostenurie
4. hipernatriurie
5. hipokaliurie
30. (1) what are the factors of patogenetici of tissue-level?

hypoxia
metabolic alkalinization
Interstitial edema
cell exicoza
cell intumescenţa
1. acidosis
metabolic alkalinization
Interstitial edema
cell exicoza
cell intumescenţa

1. acumulatrea metabolites
Interstitial edema
cell exicoza
cell intumescenţa
1. catecolaminele
2. histamine
4. aldosterone
5. acetylcholine

1. catecolaminele
2. the proinflammatory cytokines
4. aldosterone
5. acetylcholine
35. (2,4) patogenetici factors of tissue-level shock?

1. catecolaminele
4. hypoxia
5. acetylcholine
1. catecolaminele
4. 1. acidosis
5. acetylcholine
1. catecolaminele
4. (2) histamine
5. acetylcholine
1. catecolaminele
4. 1 acumulatrea metabolites.
5. acetylcholine
39. (5) What changes in microcirculation occur in compensated shock in the kidneys and
abdominal organs?
Vascular hiperpermeabilitate
edema
venous hyperemia
seizure of blood in capillaries
ischemia
40. (5) What changes in microcirculation occur in compensated shock in the kidneys and
bdominale organs?
Vascular hiperpermeabilitate
edema
venous hyperemia
spasm at the same time of pre-and postcailarelor
41. (1.5) What changes in microcirculation occur in compensated shock in the kidneys and
abdominal organs?
ischemia
edema
venous hyperemia
spasm at the same time of pre-and postcailarelor
42. (1) The changes in microcirculation occur in shock decompemsated in kidney and
abdominal organs?
1. vascular hiperpermeabilitate edema
2. at the same time of precapilarelor spasm and capillaries
3. concurrent to dilate and capillaries precapilarelor
4. precapilarelor spasm and post-dilation of capillaries
5. peripheral organ ischemia
43. (1) The changes in microcirculation occur in shock decompemsated in kidney and
abdominal organs?
1. seizure of the blood in the capillaries
2. ischemia
5 arterial hyperemia.
44. (2) What changes in microcirculation occur in shock decompemsated in kidney and
abdominal organs?
1. hyperemia pressure
2. precapilarelor with dilatation of the lingering post-spasm capillaries
5. mass ischemia
abdominal organs?
3. precapilarelor spasm and post capillary dilation
4. venous hyperemia
5. mass ischemia
abdominal organs?
3. simultaneously spasm of precapilarelor and post-capillaries
4. mass ischemia
5. Venous Stasis
47. (1.5) What changes in microcirculation occur in shock decompemsated in kidney and
abdominal organs?
1. 1. vascular hiperpermeabilitate edema
4. mass ischemia
5. Venous Stasis
abdominal organs?
1. 1. seizing blood capillaries
4. mass ischemia
5. Venous Stasis
abdominal organs?
1. 2. precapilarelor with persistent contraction expansion of post-capillaries
4. mass ischemia
5. Venous Stasis
abdominal organs?
1. 4 venous hyperemia.
4. mass ischemia
5. Venous Stasis
51. (2) What respiratory disorder occurs in the late stages of shock?
deep breath and accelerated
shallow breathing and accelerated
respiratory alkalosis with lung hyperventilation
alveolar hipoventilaţia with respiratory alkalosis
respiratory acidosis with lung hyperventilation
52. (5) the value of Dieresis renal failure can be installed in shock?
1. diuresis of 150-200 ml/hour
2. diuresis of 100-150 ml/h
3. diuresis of 50-100 ml/hour
4. excretion of 20-50 ml/HR
5. diuresis of 10-20 ml/HR
53. (1) how do I change the biochemistry of blood in shock with kidney failure?
1. ceşterea non-nitrogen concentration in the blood
2. ceşterea protein nitrogen concentration in the blood
3. increased concentration of amino acids in the blood
4. increased concentration of uric acid in the blood
5. to increase the concentration of ammonia in the blood
54. (1) how do I change the biochemistry of blood in shock with kidney failure?
1. ceşterea the concentration of urea
2. ceşterea the concentration of uric acid
3. increased concentration of amino acids
4. increased concentration of ammonia
5. increased concentration of proteins
55. (1.5) How do I change the biochemistry of blood in shock with kidney failure?
5.1. nitrogen concentration of non-ceşterea in blood
56. (1) which is the main pathogenetic link to liver failure in shock?
hipoperfuzia liver
dimiuarea glycogen in the liver
reduction of lipids in the liver
Portal hypertension
ascites
57. (2) The biochemical changes in the blood occur in shock with liver failure?
5. increased concentration of proteins
58. (3) what is the blood-intestinal injury in shock?

absorption from the intestine of bile acids
absorption from the intestine of direct bilirubin
absorption from the intestine of biogenic amines
absorption from the intestine of intestinal enzymes
intense absorption in the intestine of water and electrolytes
1. absorption from the intestine of bile acids
2. absorption from the intestine of direct bilirubin
3. absorption of bacterial endotoxins
absorption from the intestine of bowel enzimemelor

3. penetration into the bloodstream of the intestinal flora
61. (3.5) by what is intestinal barrier injury blood-in shock?
absorption from the intestine of biogenic amines
62. (3.5) by what is intestinal barrier injury blood-in shock?
3. absorption of bacterial endotoxins
63. (3) pancreatic lesions manifested in shock?

1. hiposeceţia insulin
3. the presence of the pancreas into the blood
4. the presence of autoantibodies antipamcreatici
5. the presence of lymphocytes sensitized antipancreatice
3. pancreatic enzymes autoactivarea
4. the presence of autoantibodies antipamcreatici
5. the presence of lymphocytes sensitized antipancreatice
3. the collapse of the arterial
5. sequential hipoinsulinismului hyperglycemia
66. (4) what is pancreatic lesions in shock?
1. hiposeceţia of insulin by the pancreas endocrine
2. hiposeceţia glucagonului by the endocrine pancreas
4. lipid necrosis
5. the presence of autoantibodies antipancreatici
67. (3,4) what is pancreatic lesions in shock?
3. (3) the presence of pancreas in the blood
4. lipid necrosis
3. pancreatic enzymes autoactivarea 3.
4. lipid necrosis
3. 3 the arterial collapse.
4. lipid necrosis
70. (2) Which is the main pathogenetic link myocardial lesions in shock?
the relative lack of coronary artery
low blood pressure in the bulb of the aorta
blood stasis in myocardium
coronary artery embolism
coronary spasm
71. (4) what is the myocardium injury in shock?
1. myocarditis
2. miocardioscleroză
3. miocardiodistrofie
4. myocardial infarction
5. anevrizm
72. (1) The value of blood glucose is incompatible with the normal activity of the brain?
2.5 mmol/L
3.5 mmol/l
10 mmol/L
100 mmol/L
500 mmol/L
73. (1) The value of oxemiei is not compatible with the normal activity of the brain?
1.20 mm Hg
2.50 mm Hg
3.100 g
4.150 m Hg
5.200 mm Hg
74. (3) The value of blood plasma osmolarity is incompatible with the normal activity of the
brain?
1. 150 mosm per/l
2. 300 mosm per/l
3. mosm per 500/l
4. 1000 mosm per/l
5. 1500 mosm per/l
75. (3) The value of body temperature is incompatible with the normal activity of the
brain?
1.36.5 C
2.35 C
3.32 C
4.38 C
5.39 C
76. (3) electrolytic dishomeostazie can cause heart failure?

Hipernatriemia
hyponatriemia associated
hyperkalemia
hipercalciemia
hiporcalciemia
77. (3) what is the sequence of terminals?

disease, preagonia, agony, clinical, biological death death
the occupations disease, preagonia, agony, clinical, biological death death
preagonia agony, death, clinical, biological death
preagonia, agony, death, postreanimaţională, biological death status
the agony of death, the death of biological
78. (3) Which is the minimum level of cerebral perfusion for resuscitation of clinical death?
10-15 ml/min/100 g
5-6 ml/100 g/min
8-10 ml/100 g/min
15-20 ml/100 g/min
25-30 ml/min/100 g
79. (1) the disturbance of nerve structures which function causes the agony?
the spinal bulb
the frontal lobe of the brain
the hypothalamus
hipocampului
the cerebral cortex
80. (3) clinical sign which is characterizing the agony?

dispneia inspiratorie
bradycardia
rare with breath descrescândă amplitude
shallow breathing and accelerated
paroxysmal
81. (4) Which is one of the signs of clinical death?

loss of consciousness
lack of cndţionate reflexes
areflexia-General
stopping the heart contractions
keeping the reflex of the pupil to light
82. (5) which is one of the clinical signs dn?
1. loss of consciousness
2. no reflexes cndţionate
3. General areflexia
4. keeping the reflex of the pupil to light
5. respiratory failure
83. (3.5) Which are signs of clinical death?
1. loss of consciousness
2. no reflexes cndţionate
3. stopping of heart contractions
4. keeping the reflex of the pupil to light
5. respiratory failure
84. (2) What factors determine the duration of clinical death?

hereditary predisposition
resistance to hypoxia cerebral cortex
the properties of tanatogeni
the reactivity of the organism
proseselor depth of arousal and înhibiţie from cover
85. (3) how long after the death of first clinical functional disorders corticali neurons?
2-3 minutes
15-30 minutes
a few seconds
5-6 minutes
45 minutes
86. (4) Over how long after installing anoxemiei corticali neurons necrosis occurs?
2-3 minutes
15-30 minutes
a few seconds
5-6 minutes
45 minutes
87. (2) how long resistant to subcortical structures anoxemie?

2-3 minutes
15-30 minutes
a few seconds
5-6 minutes
45 minutes
88. (1) what is the duration of the extension mechanism of clinical death in hypothermia?
biochemical reactions and speed reduction of the oxygen consumption
bradycardia caused by low temperature
Start Adaptive reactions at low temperatures
decreased respiratory coefficient
increasing the efficiency of biological oxidation
Secială pathophysiology
(I). Central nervous system (62)
1. What is the extent of cell excitability?
a. resting potential value

b. the critical value of the membrane potential
c. #diferenţa of the potential and critical value of resting potential
d. depolarizării slow speed
e. deplarizării quick speed
2. What is the threshold of excitation of the excitable cell?
1. the minimum value of excitantului which initiates the slow depolarizarea

2. minimum excitantului #valoarea that depolarizează membrane up to the critical
value
3. the minimum value of excitantului which annihilates the potential mebranar
4. the minimum value of the membrane potential excitantului that inverts
5. the minimum value of excitantului which produce membrane hiperpolarizarea
3. How do I change cell excitability to decrease the potential for sleep?

6. #excitabilitatea increase
7. decreases excitability
8. excitability is not changed
9. the inhibition occurs hiperpolarizantă
10. loose cell excitability
3. How to change cell excitability in increased potential for sleep?
1. excitability increases
2. #excitabilitatea falls
3. excitability is not changed
4. the inhibition occurs depolarizantă
5. loose cell excitability
4. The process increases the excitability of the cell?
1. #hipoxia
2. optimal oxygenation
3. optimum nutrition
4. increasing the intracellular ATP
5. increased concentration of extracellular Na
5. The process increases the excitability cell grow?
1. #hiponutriţia

1. #acidoza

1. #inflamaţia

2. #scăderea intracellular ATP

1. increased extracellular K #concentraţia
2. low concentration of extracellular K
4. increased concentration of extracellular Ca
10. What processes are increasing cell excitability?

2. scăută of extracellular Na #concentraţia
4. lowering the intracellular ATP

3. increased intracellular Na #concentraţia
12. How do I change the cell resting potential of excitable membrane pumps according to Na,
K?
1. #depolarizare
2. Repolarization
3. inversion of potential
4. hyperpolarization
5. does not change
13. How to modify the intracellular concentration of electrolytes from membrane pumps
according to Na, K?
1. increase the concentration of K and Na
2. decreases the concentration of K and Na
3. #creşte concentration of Na concenraţia K decreases;
4. decreases the concentration of Na concntaţia K increases;
5. increase the concentration of Na, K concentration does not change
14. How does membrane pumps, cessation of Ca, Mg on The intracellular homeostasis?
1. increase the concentration of Ca in reticulum reticulum
2. decreases the concentration of Ca in reticulum reticulum
3. #creşte concentration of Ca in hialoplasmă
4. decreases the concentration of Ca in hialoplasmă
5. increase the concentration of Ca in the reticulum and hialoplasmă reticulum
15. What is the mechanism of action of excitanţi mediators?
1. #deschid Na channels
2. Open The channels
3. Open Cl channels
4. Open the channels of H
5. blocking channels As
16. What is the mechanism of action of mediators as histamine?
1. Open the channels of Na

2. Open The channels
3. #deschid Cl channels
4. Open the channels of H
5. blocking channels As
17. What is the mechanism of încondiţii cell excitability increase hypoxia?
1. energy restriction #deficitul Na, K pump depolarization;

2. energy shortages; according to Na, K pump, intracellular concentration of ceşterea
As
3. energy shortages; according to Na, K pump, reduction of membrane potential
critical value
4. energy shortages; according to Na, K pump, increased concentration of intracellular
Cl
5. energy shortages; according to Na, K pump, increase intracellular concentration of
K
18. What is the mechanism excitability cell growth in hiponutriţie?
1. energy restriction #deficitul Na, K pump depolarization;

2. energy shortages; according to Na, K pump, intracellular concentration of ceşterea
As
3. energy shortages; according to Na, K pump, reduction of membrane potential
critical value
4. energy shortages; according to Na, K pump, increased concentration of intracellular
Cl
5. energy shortages; according to Na, K pump, increase intracellular concentration of
K
19. What is the effect of blocking the receptor postsinaptici?

1. hiperfuncţia innervated structures
2. innervated structures atrophy
3. hipersensibilizarea innervated structures
4. desensitization innervated structures
5. #paralizia innervated structures
20. What is the effect of the mediator reserves in terminaţiunile nerve?
1. mediator synthesis stimulation exhausted

2. #hipoactivitatea structure of postsynaptic
3. hyperactivity postsynaptic structures
4. stimulating effects of mediator antagonists
5. inactivation of degrading enzimeleor Ombudsman
21. What is the effect of norepinephrine in reserves terminaţiunile postsynaptic sympathetic?
1. #hipotensiune pressure
2. hypertension
3. muscular hypotonia
4. muscle hipertonus
5. parkinsonian tremor
22. What is the effect of dopamine in reserves extrapiramidali endings?
1. a. hypotension
2. hypertension
3. muscular hypotonia
4. muscle hipertonus
5. parkinsonian-#tremor
23. The affection which the spastic paralysis occurs structures?
1. chines motoneuronii
2. #motoneuronii corticali
3. extrapyramidal system motoneuronii
4. spinal motor nerves
5. the discovery of spinal nerves
24. The affection which the spastic paralysis occurs structures?
1. chines motoneuronii
3. spinal motor nerves
4. #tractul corticospinal fibers
5. the discovery of bulbari nerves
25. The affection which the flaccid paralysis occurs structures?
1. chines #motoneuronii
2. motoneuronii corticali
26. The affection which the flaccid paralysis occurs structures?

2. #nervii spinal motor
3. the corticospinal fibers
4. the discovery of bulbari nerves
27. What characterizes the spastic paralysis?

1. loss of involuntary movements
2. #pierderea voluntary movements
3. loss of automatic movements
4. loss of conditioned reflexes
5. the loss of the unconditioned reflex

How do I change muscle tone in spastic paralysis?
1. hipotonusul skeletal muscles
2. hipertonusul skeletal muscles
3. skeletal muscle atrophy

How to change motor reflexes in spastic paralysis?
1. keeping the intensity of normal spinal reflexes
2. spinal #hiperreflexie
3. loss of spinal reflex
30. What characterizes the flaccid paralysis?
1. keeping the intensity of normal spinal reflexes

2. spinal hiperreflexie
3. #pierderea spinal reflex

1. loss of involuntary movements with keeping those voluntary
2. loss of voluntary movement with keeping those involuntary
3. #pierderea voluntary movements and involuntary ones
4. loss of automatic movements

1. #hipotonusul skeletal muscles
3. hipererflexie
1. #atrofia skeletal muscles
3. skeletal muscle atrophy
34. What is the physiological pain?

1. nocigen stimulus action appears on exteroreceptorilor
2. #apare to nocigen over nocireceptorilor stimulus
3. nocigen stimulus action appears on proprioreceptorilor
4. occurs spontaneously, in the absence of stimulus nocigen
5. the stimulus physiological action appears on nociceptorilor
35. What is the physiological pain?
1. excitation threshold is increased and the sensation of pain intensity decreases

2. the threshold of excitation is reduced and the intensity of the sensation of pain
increases
3. excitation #pragul is normal and the intensity of the sensation of pain is adequate
excitantului
4. excitation threshold is increased and the intensity of the sensation of pain increases
5. the threshold of excitation is reduced and the sensation of pain intensity decreases
36. What characterises the pathological pain?
1. excitation threshold is increased and the sensation of pain intensity decreases

2. #pragul of excitation is reduced and the intensity of the sensation of pain increases
3. the threshold of excitation is normal and the intensity of the sensation of pain is
adequate excitantului
4. excitation threshold is increased and the intensity of the sensation of pain increases
5. the threshold of excitation is reduced and the sensation of pain intensity decreases
37. What characterises the pathological pain?
1. occurs at specific excitation nociceptorilor

2. occurs at specific excitation of nociceptive system structures
3. #apare to the location of the pathological processes in the structures of the
nociceptive system
4. occurs in the posterior horns of spinal distrucţia
5. the Cingulate gyrus postcentral cortical distrucţia
38. What is the mechanism of the pain to the anoxia organ?
1. synthesis of kininelor nocigene

2. #acumularea cataboliţilor anaerobi
3. direct excitation of the nocigeni receptor for lack of oxygen
4. the reduction of the threshold for excitaţâie to nociceptorilor
5. sensitizarea nociceptorilor
39. What is the mechanism of the pain to the spastic contraction of smooth muscles of
internal organs?
1. synthesis of kininelor nocigene

2. cataboliţilor anaerobi accumulation
3. mechanical receptor nocigeni #excitarea
40. What is the mechanism of pain in the body's inflammation?
1. #sinteza kininelor nocigene

2. cataboliţilor anaerobi accumulation
3. direct excitation of the nocigeni receptor
41. Suprasegmentar is the answer to pain?
1. increased parasympathetic tone and Autonomic system

2. autonomic system sympathetic tone #creşterea
3. autonomic system sympathetic tone reduction
4. reducing sympathetic autonomic system tone and parasympathetic
5. autonomic system tone increase sympathetic and parasympathetic
42. The cardiovascular system is the answer to pain?
1. tachycardia and hypotension

2. bradycardia and hypotension
3. #tahicardie and hypertension
4. bradycardia and hypertension
5. tachycardia and decreasing peripheral circulation resistance
43. Endocriin system is the answer to pain?
1. hipersecreţia medulosuprarenalelor, corticosuprarenalelor, thyroid and insulin

2. #hipersecreţia medulosuprarenalelor, corticosuprarenalelor, glucgonului
3. hipersecreţia medulosuprarenalelor corticosuprarenalelor, hipopsecreţia, thyroid
and insulin
4. hipersecreţia medulosuprarenalelor, corticosuprarenalelor, sexuaţi and insulin
hormone
5. medulosuprarenalelor, corticosuprarenalelor, hipersecreţia reducing the secretion of
hormones sexuaţi
44. What is the function of antinociceptiv?
1. annihilates any sensation of pain

2. decreases any feeling of pain
3. just a diminishes the physiological pain sensation
4. #diminuează just the sensation of pathological pain
5. diminish chronic pain?
45. What is the effect of sympathetic autonomic system upon activation of carbohydrate
metabolism?
1. activating glicoligenogenezei with hypoglycemia
2. #activarea glicogenolizei with hyperglycemia
3. turn on neoglucogenezei
4. activation of carbohydrate oxidation in the Krebs Cycle
5. lipogenezei activation of glucose
46. What is the effect of autonomic sympathetic system activation of lipid metabolism?
1. lipogenezei activation of glucose

2. activation of lipid oxidation in the Krebs Cycle
3. activation of beta oxidation of fatty acids
4. #activarea lipolizei with hyperlipidemia of transport
5. turn on processing fatty acids into glucose
47. What is the effect of simpaticotrop on the endocrine glands?
1. #activarea endocrine axis hypothalamus-adenohipofiză-corticosuprarenale-

glucocorticosteroizi
2. activation of endocrine axis hypothalamus-adenohipofiză-corticosuprarenale-
mineralocorticosteroizi
3. activation of endocrine axis hypothalamus-adenohipofgiză-thyroid-thyroxine
4. activation of endocrine axis hypothalamus-adenohipofiză-sexuaţi-hormones gonads
5. activation of endocrine axis hypothalamus-adenohipofgiză-somatrophin
48. What is the effect of simpaticotrop on cardiovascular system?

1. #efecte cardiotrope positive-increased cardiac output-high blood pressure
2. cardiotrope negative effects decreasing cardiac output-low blood pressure
3. cardiotrope positive effects-increased cardiac output-hypertension-increased
skeletal muscle perfusion at rest-ischemia myocardium
4. cardiotrope negative effects decreasing cardiac output-low blood pressure-reducing
skeletal muscle perfusion, myocardial ischemia
49. What is the effect of simpaticotrop upon the digestive tract?
1. stimulating digestive glands-tonicităţii smooth muscle stimulation-stimulating the
motility-stimulating food bowl-easing passage sfincterilor
2. #inhibiţia digestive gland secretion-smooth muscle relaxation-inhibition of
motility-the Bowl food passage retardation-sfincterilor spasm
3. inhibition of secretion of digestive glands-smooth muscle relaxation-inhibition of
motility-the Bowl food passage retardation-relaxation sfincterilor
4. stimulating digestive glands-smooth muscle relaxation-inhibition of motility-
stimulating food bowl-easing passage sfincterilor
5. sinhibiţia digestive gland secretion-tonicităţii smooth muscle stimulation-
stimulating the motility-stimulating food bowl-passage sfincterilor spasm
50. What is the simpaticotrop of the bronhial tree?

1. the spasm smooth muscles of the bronchi, obstructive hipoventilaţie, mucozală
hypersecretion
2. the spasm smooth muscles of the bronchi, hipoventilaţie obstructive, hiposecreţie
mucozală
3. relaxing the smooth muscles of the bronchi, obstructive hipoventilaţie, mucozală
hypersecretion
4. smooth #relaxarea of the bronchi, the reduction of aeroconductorii resistance,
inhibition of mucozale secretion
5. the spasm smooth muscles of the bronchi, the reduction of aeroconductorii
resistance, inhibition of mucozale secretion
51. What is the simpaticotriop simpaticotrop of the coronary blood vessels?
1. vessels with alpha-adrenergic innervation is spasmează
2. vessels with alpha-adrenergic innervation expands
3. vessels with beta-adrenergic innervation is spasmează
5. vessel spasm with innervation and beta-alpha-adrenergic
52. What is the effect of simpaticotrop on the blood vessels of the abdominal organs?
1. vessels with alpha-adrenergic innervation is spasmează
3. vessels with beta-adrenergic innervation is spasmează
5. abdominal organs do not have vessels innervation sympathy
53. What is the effect of simpaticotrop on the external sexual organs?
1. spasm arterioles corpora cavernoşi-venulelor corpora cavernoşi spasm-ductus

deferens contraction-contraction of the seminal vesicle-emission, ejaculation
2. dilation of arterioles corpora cavernoşi-venulelor corpora cavernoşi spasm-ductus
deferens contraction-contraction of the seminal vesicle-erection
3. #spasmul corpora cavernoşi arterioles-venulelor corpora cavernoşi spasm-deferens
duct relaxation-relaxation of seminal vesicle-emission, ejaculation
54. What are the effects of simaticotrope on the eye?
1. #contracţia dilatatorului pupil, ciliary muscle relaxation-midriaz, aplatisiarea lens-

presbitism
2. dilatatorului contraction of the pupil, ciliary muscle contraction-midriaz, sferizarea
lens-accommodation, myopia
3. relaxation dilatatorului relaxation ciliary muscle-pupil, lens sferizarea-
accommodation, myopia
5. dilatatorului contraction of the pupil, ciliary muscle relaxation-midriaz, sferizarea
55. What are the effects of simpaticotrope on the eye?
1. miosis, sferizarea lens, lacrimaţie

2. #midriaza, aplatisarea, lacrimaţie lens
3. miosis, aplatisarea lens, lacrimal secretion inhibition
4. midriaza, sferizarea, inhibition of lacrimaţiei lens
5. midriaza, aplatisarea, inhibition of lacrimaţiei lens
56. What are the effects of simpaticotrope on vessels and skin derivatives?
a. vessel-constricting sweat glands secretion-airway constriction of muscles

piloerectori
b. reduction of vessels constricting sweat glands secretion-relaxation of muscles
piloerectori
c. dilating-glandelr sweat secretion-airway constriction of muscles piloerectori
d. dilating-secretion of the sweat glands-constricting muscles piloerectori
e. constricting vessels-decreasing the secretion of sweat glands, muscle-relaxation
piloerectori
57. What is the effect of parasimpaticotrop on cardiovascular system?
1. cardiotrope positive effects-increased cardiac output-high blood pressure

2. cardiotrope negative #efecte-decrease cardiac output-low blood pressure
4. cardiotrope negative effects decreasing cardiac output-low blood pressure-reducing
skeletal muscle perfusion, myocardial ischemia
58. What is the effect of the parasimpaticotrop effect on the digestive tract?
1. #stimularea digestive gland secretion-tonicităţii smooth muscle stimulation-
stimulating the motility-stimulating food bowl-easing passage sfincterilor
motility-the Bowl food passage retardation-sfincterilor spasm
motility-the Bowl food passage retardation-relaxation sfincterilor
4. stimulating digestive glands-smooth muscle relaxation-inhibition of motility-
stimulating food bowl-easing passage sfincterilor
5. sinhibiţia digestive gland secretion-tonicităţii smooth muscle stimulation-
stimulating the motility-stimulating food bowl-passage sfincterilor spasm
59. What is the effect of parasimpaticotrop on the effect of bronhial tree?

1. #spasmul smooth muscles of the bronchi, obstructive hipoventilaţie, mucozală
hypersecretion
2. the spasm smooth muscles of the bronchi, hipoventilaţie obstructive, hiposecreţie
mucozală
3. relaxing the smooth muscles of the bronchi, obstructive hipoventilaţie, mucozală
hypersecretion
4. smooth relaxation of bronchi, reducing the resistance of the aeroconductorii,
inhibition of mucozale secretion
5. the spasm smooth muscles of the bronchi, the reduction of aeroconductorii
resistance, inhibition of mucozale secretion
60. What is the effect of the parasimpaticotrop effect of the external sexual organs?

deferens contraction-contraction of the seminal vesicle-emission, ejaculation
2. #dilatarea corpora cavernoşi arterioles-venulelor corpora cavernoşi spasm-erection
3. spasm arterioles corpora cavernoşi-venulelor corpora cavernoşi spasm-deferens
duct relaxation-relaxation of seminal vesicle-emission, ejaculation
61. What are the effects of parasimaticotrope on the eye?

1. dilatatorului contraction of the pupil, ciliary muscle relaxation-midriaz, aplatisiarea
lens-presbitism
3. relaxation dilatatorului relaxation ciliary muscle-pupil, lens sferizarea-
accommodation, myopia
4. #contracţia sphincter constriction of the pupil, ciliary muscle, contraction-sferizarea
5. dilatatorului contraction of the pupil, ciliary muscle relaxation-midriaz, sferizarea
62. What are the effects of parasimpaticotrope on the eye?

1. miosis, sferizarea lens, lacrimaţie
2. midriaza, aplatisarea, lacrimaţie lens
3. #mioza, aplatisarea, inhibition of lacrimal secretion lens
4. midriaza, sferizarea, inhibition of lacrimaţiei lens
5. midriaza, aplatisarea, inhibition of lacrimaţiei lens
2. endocrine system (160)
1. What is the cause dysregulation of the adenohipofizei function?
a. the disturbance of hypothalamic liberinelor to adenohipofiză transport

through systemic circulation
(b). #dereglarea liberinelor transport adenohipofiză to the hypothalamic
Portal circulation hipfizară
(c). disruption of axonal transport of hypothalamic liberinelor adenohipofiză
views
(d). hypothalamic malfunction inervaţiei of adenohipofizei
(e). disturbance of the relationship between adenohipofiză and neurohipofiză
2. What is the cause dysregulation of the adenohipofizei function?

(b). #dereglarea synthesis of adenohipofiză through liberinelor hypothalamic
towards Portal circulation hipfizară
views
(e). disturbance of the relationship between adenohipofiză and neurohipofiză
3. What causes the disorder adenohipofizei function?

(b). #dereglarea liberinelor transport adenohipofiză to the hypothalamic
Portal circulation hipfizară
views
(e). #liberinelor hypothalamic malfunction transport to adenohipofiză
through hipfizară Portal circulation
4. What is the cause of hipersecreţiei antidiuretic hormone?
a. blood plasma izoosmolaritatea

(b). blood plasma #hiperosmolaritatea
(c). blood plasma hiposmolaritatea
(d). hyponatriemia associated
(e). hyperkalemia
5. What is the cause of hipersecreţiei antidiuretic hormone?

(b). #hipernatriemia
(d). hyponatriemia associated
(e). hyperkalemia
6. What are thecauses of hyperantidiuretic hormone secretion?

(b). blood plasma #hiperosmolaritatea
(d). #hipernatriemia
(e). hyperkalemia
7. What is the mechanism of hiposecreţiei antidiuretic hormone from pituitary
presser foot trauma?
a. discontinue carriage of hypothalamic liberinelor to adenohipofiză via port

adenoma
(b). discontinue carriage of antidiuretic hormone from the hypothalamus to
the pituitary via the adenohipofiză port
(c). #se interrupt the transport of antidiuretic hormone from the
hypothalamus to the plates there axonii neurohipofiză
(d). discontinue carriage of antidiuretic hormone from the hypothalamus to
the pituitary via the adenohipofiză port
(e). neurogenic stimulation is interrupted to the hypothalamus hypophysis
8. What is hipersecreţia ADH?
a. #oliguria
(b). poliuria
(c). izostenuria
(d). polakiuria
(e). dizuria
9. What is hipersecreţia ADH?
a. oliguria
(b). poliuria
(c). #hiperstenuria
(d). polakiuria
(e). dizuria
10. What are the manifestations of hiposecreţiei ADH?
a. #oliguria
(b). poliuria
(c). #hiperstenuria
(d). polakiuria
(e). dizuria
11. What is the cause of hipersecreţiei prolactin?
a. hipersecreţia pituitary lactoliberinei

(b). hipersecreţia pituitary lactostatinei
(c). discontinuation of pituitary lactostatinei adenohipofiză views
(d). #întreruperea pituitary dopamine transport to adenohipofiză
(e). interruption of the pituitary to norepinephrine adenohipofiză transport
12. What is the cause of hipersecreţiei prolactin?

a. #adenom acidophilic pituitary cells
(b). pituitary adenoma cells basophils
(c). pituitary adenoma cells cromofobe
(d). afenom neurohipofizar
(e). pituitary intermediate lobe of the pituitary gland
13. What are the causes of hipersecreţiei prolactin?
a. #adenom acidophilic pituitary cells

(b). pituitary adenoma cells basophils
(c). pituitary adenoma cells cromofobe
(d). afenom neurohipofizar
(e). #întreruperea pituitary dopamine transport to adenohipofiză
14. What is hipersecreţia prolactin in women?
a. #Amenoree
(b). #sterilitate
(c). hipogalactie
(d). #lactoree
(e). Mamre glands Atrophy
a. #Amenoree
(b). hipogalactie
(c). Gynecomastia
(d). hypersexuality
(e). hirsutism
a. hipogalactie
(b). #lactoree
(c). hypersexuality
(d). hirsutism
(e). glanelor breast atrophy
a. #sterilitate
(b). hipogalactie
(c). hypersexuality
(d). hirsutism
(e). glanelor breast atrophy
18. What is hipersecreţia prolactin in men?
a. #ginecomastie
(b). hypersexuality
(c). hirsutism
(d). #oligozoospermie
(e). #diminuarea libido
a. #oligozoospermie
(b). hypersexuality
(c). hirsutism
(d). obesity
(e). her gigantism
a. #diminuarea libido
(b). hypersexuality
(c). hirsutism
(d). obesity
(e). her gigantism
a. #ginecomastie
(b). hypersexuality
(c). hirsutism
(d). obesity
(e). her gigantism
22. What is the mechanism to lactotrop hormone hipersecreţiei presser foot trauma
adenoma?
a. discontinue carriage of hypothalamic lactostatinei to adenohipofiză via

port adenoma
(b). discontinue carriage of lactotrop hormone from the hypothalamus to the
pituitary via the adenohipofiză port
(c). discontinue carriage of lactotrop hormone from the hypothalamus to the
plates there axonii neurohipofiză
(d). #se întrrupe transport of dopamine from the hypothalamus to the
pituitary Portal circulation adnohipofiză
(e). întensifică neurogenic stimulation of the pituitary gland by the
hypothalamus
23. What causes hipersecreţiei somatotropic hormone?
a. hipersecreţia long-acting somatostatin

b. hipersercreţia somatomedinelor
c. hiposecreţia somatomedinei
d. #hipersecreţia somatoliberinei
e. hipersecreţia glucagonului
a. pituitary adenoma bazofil

b. #adenom adenoma acidofil
c. pituitary adenoma cromofob
d. pituitary posterior lobe of the hypophysis
e. pituitary intermediate lobe of the pituitary gland
f. pituitary adenoma bazofil

g. #adenom adenoma acidofil
h. pituitary adenoma cromofob
i. pituitary posterior lobe of the hypophysis
j. #hipersecreţia somatoliberinei
26. What causes hiposecreţiei somatotropic hormone?
a. #hiposecreţia long-acting somatostatin

(b). hipersercreţia somatomedinelor
(c). hiposecreţia somatomedinei
(d). hipersecreţia somatoliberinei
(e). hiposecreţia glucagonului
a. pituitary basophils cells atrophy

b. #atrofia acidophilic pituitary cells
c. pituitary cells atrophy cromofobe
d. păosterior lobe of the pituitary gland atrophy
e. the intermediate lobe of the pituitary gland atrophy
f. pituitary basophils cells atrophy

g. #atrofia acidophilic pituitary cells
h. pituitary cells atrophy cromofobe
i. păosterior lobe of the pituitary gland atrophy
1. #hiposecreţia long-acting somatostatin
29. How to change carbohydrate metabolism in hipersecreţia bovine somatotrophin in

children?
a. glicogenogeneza intensifies with hypoglycemia

b. #se glicogenoliza intensifies with hyperglycemia
c. gluconeogeneza intensifies
d. decreases gluconeogeneza
e. decreases glicogenoliza with hypoglycemia
30. How do I change the protein metabolism in bovine somatotrophin hipersecreţia?
a. proteoliza intensifies the negative nitrogen balance

b. transaminarea amioacizilor intensifies
c. #se proteosinteza with positive balance boosts nitrogen
d. Conentraţia increase of ammonia in the blood
e. Increases in blood urea cocentraţia
31. How do I change the biochemistry of blood in the hipersecreţia of somatrophin?
a. hyperglycemia, hierlipidemie, ketonaemic

(b). hoperglicemie, hipolipidemie, hipercetonemie
(c). hypoglycemia, Hyperlipidemia, without ketonaemic
(d). hypoglycaemia, hipolipidemie, ketonaemic
(e). #hiperglicemie, Hyperlipidemia, hipercetonemie
32. What are somatic manifestations in bovine somatotrophin in children

hipersecreţia?
a. her gigantism, acromegaly, splanhnomegalie

(b). #gigantism, splanhnomegalie
(c). acromegaly, splanhnomegalie
(d). her gigantism, acromegaly
(e). acromegaly, atrophy of the internal organs
33. What are somatic manifestations in adult somatotrophin hipersecreţia?
a. her gigantism, acromegaly, splanhnomegalie

(b). her gigantism, splanhnomegalie
(c). #acromegalie, splanhnomegalie
(d). her gigantism, acromegaly
(e). acromegaly, atrophy of the internal organs
34. What are somatic manifestations in adult somatotrophin hiposecreţia?
a. dwarfism, fetus hypotrophy, internal organs, osteopenia, connective tissue

atrophy
(b). her gigantism, fetus hypotrophy, internal organs, osteopenia, connective
tissue atrophy
(c). #hipotrofia internal organs, osteopenia, connective tissue atrophy
(d). acromegalia, fetus hypotrophy, internal organs, osteopenia, connective
tissue atrophy
(e). dwarfism, splanhnomegalia, osteopenia, connective tissue atrophy
35. What are somatic manifestations in bovine somatotrophin in children

hiposecreţia?
a. #nanism, internal organs, osteopenia hypotrophy, atrophy of connective

tissue
(b). her gigantism, fetus hypotrophy, internal organs, osteopenia, connective
tissue atrophy
(c). internal organs hypotrophy, atrophy, connective tissue osteopenia
(d). acromegalia, fetus hypotrophy, internal organs, osteopenia, connective
tissue atrophy
(e). dwarfism, splanhnomegalia, osteopenia, connective tissue atrophy
Corticosuprarenalele
36. What is the cause of the tertiary hipercorticismului?
a. #hipersecreţia corticoliberinei
(b). hiposecreţia corticoliberinei
(c). hipersecreţia corticotropinei
(d). hiposecreţia corticotropinei
(e). direct settlement of corticosuprarenalelor disordering
37. What is the cause of possible secondary hipercorticismului?
a. hipersecreţia corticoliberinei
(b). hiposecreţia corticoliberinei
(c). #hipersecreţia corticotropinei
(d). hiposecreţia corticotropinei
(e). direct settlement of corticosuprarenalelor disordering
38. What is the cause of primary hipercorticismului?
a. hormonsecretoare tumor of the hypothalamus

(b). hormonsecretoare of adenohipofizei tumor
(c). hormonsecretoare to #tumoare to corticosuprarenalelor
(d). direct settlement of corticosuprarenalelor disordering
(e). frustration adjustment feed back to corticosuprarenalelor
39. What is the cause of the tertiary hipocorticismului?
a. #hiposecreţia corticoliberinei
(b). pituitary gland atrophy
(c). direct settlement of corticosuprarenalelor disordering
(d). frustration adjustment feed back to corticosuprarenalelor
(e). corticosuprarenalelor atrophy
40. What is the cause of possible secondary hipocorticismului?
a. hiposecreţia corticoliberinei
(e). corticosuprarenalelor atrophy
41. What is the cause of primary hipcorticismului?
a. hiposecreţia corticoliberinei
(e). #atrofia corticosuprarenalelor
42. What is the mechanism of prolonged administration of corticosuprarenalelor

hiposecreţiei in large doses of glucocorticosteroizilor?
a. glucocorticosteroizii exogenous adrenal cortex directly inhibit

(b). #glucocorticosteroizii external inhibit the secretion corticotropinei
(c). glucocorticosteroizii external inhibit the secretion of adrenal cortex and
corticoliberinei
(d). glucocorticosteroizii external inhibit the secretion of adrenal cortex and
somatotrophin
(e). exogenous desensitizează glucocorticosteroizii receptors for endogenous
steroids
43. What is the mechanism of Leydig cells from prolonged high-dose administration
of androgenelor?
a. exogenous directly inhibits the multiplication of androgenele cells, Leydig
(b). exogenous inhibits secretion of LH #androgenele
(c). exogenous inhibits FSH secretion androgenele
(d). androgenele inhibits secretion inhibits exogenous bovine somatotrophin
(e). androgenele exogenous and endogenous desensitizează receptors for
androsteroizii
44. What is the mechanism of Sertoli cells from prolonged high-dose administration
of androgenelor?
a. exogenous directly inhibits the multiplication of androgenele cells, Leydig

(b). exogenous inhibits secretion of LH androgenele
(c). exogenous inhibits FSH secretion #androgenele
(d). androgenele inhibits secretion inhibits exogenous bovine somatotrophin
androsteroizii
45. What is the mechanism of prolonged administration of testosterone hiposecreţiei

in large doses of androgenelor?
a. exogenous androgenele androgenelor secretion directly inhibits the Leydig

cells
(b). exogenous LH secretion inhibits #androgenele which subsequently
inhibits Leydig cells inhibit the secretion
(c). exogenous FSH secretion inhibits androgenele which subsequently
inhibits the secretion of Leydig cells
(d). exogenous androgenele inhibits secretion of bovine somatotrophin
which subsequently inhibits the secretion of Leydig cells
androsteroizii
46. What is hipersecreţia glucocorticosteroizilor?
a. #osteoporoză
(b). #pierderea calcium in the bones
(c). hipocalciemie
(d). #hipercalciemie
(e). exaggerated bone calcification

a. #hipotensiune pressure
(b). hypertension
(c). bradycardia
(d). perifarice resistance of #diminuarea blood circulation
(e). arteriolar tone #diminuarea
a. thymus hyperplasia
(b). thymus #atrofia and lymphoid tissue
(c). limfocitoză T lymphocytes
(d). limfocitoză with B lymphocytes
(e). #predispoziţia in allergic diseases
a. gastric hipoaciditate
(b). gastric #ulcerogeneză
(c). enhancement of proliferation of gastric mucosa hypertrophy with
epiteliocitelor
(d). gastrin secretion #intensificarea
(e). increased secretion of histamine
a. increase resistance to infectious diseases

(b). #diminuarea resistance to infectious diseases
(c). allergic diseases #predispoziţia
(d). predisposition to the diseases parasitic
(e). limfocitoză
a. hypoglycemia
(b). #hiperglicemie
(c). increased glucose tolerance
(d). low glucose #toleranţa
(e). #hipersecreţia insulin
a. hypoglycemia
(b). #hiperlipidemie
(c). hiperproteinemie
(d). low carbohydrate #toleranţa
(e). #hipersecreţia insulin
53. What are the metabolic effects of glucocorticosteroizilor?
a. increase proteosinteza
(b). lipogeneza falls
(c). glicogenogeneza intensifies
(d). #se enhances gluconeogeneza
(e). #Se intensifies the lipolysis
54. What are the manifestations of hipersecreţiei glucocorticosteroizilor?
a. limfocitoză T lymphocytes
(b). limfocitoză with B lymphocytes
(c). #limfocitopenie
(d). #eozinopenie
(e). thymus hyperplasia
a. #hiposecreţia gonadoliberinei
(b). #hiposexualitate
(c). hipersecreţia LH
(d). hipersecreţia FSH
(e). hypersexuality
a. General Obesity
(b). #obezitatea trunk body
(c). caşexie
(d). muscle #hipotrofie
(e). the "Hippocratic"
57. What are the manifestations of hiposecreţiei glucocorticosteroizilor?
a. hypertensive crisis
(b). #colaps arteriosus
(c). tachycardia
(d). increasing resistance of peripheral blood circulation
(e). increased arteriolar tone
58. What are the manifestations of hiposecreţiei glucocorticosteroizilor?
a. cardiac #insuficienţă
(b). hypertension
(c). bradycardia
(d). increasing resistance of peripheral blood circulation
(e). increased arteriolar tone
59. What are the manifestations of primary hiposecreţiei to glucocorticosteroizilor?
a. hiposecreţie of corticosteroids
(b). #hipersecreţia of ACTH
(c). hiposecreţia of POMC
(d). skin #hiperpigmentaţia
(e). insufiicienţa melanin
60. What are the manifestations of glucocorticosteroizilor side hiposecreţiei?
a. #hiposecreţie of ACTH
(b). hipersecreţia of ACTH
(c). #de corticosteroids
(d). skin hiperpigmentaţia
(e). excess melanin
61. What is the primary cause of hiperaldosteronismului?
a. #tumoarea hormonsecretoare layer of glomerulus Nr.38

(b). hormonsecretoare tumor of the fasciculat layer of Nr.38
(c). hormonsecretoare tumor of the layer of cross-linked Nr.38
(d). tumor hormonsecretoare in adenohipohiză
(e). tumor hormonsecretoare in hippotalamus
62. What are the causes of secondary hiperaldosteronismului?

a. paroxysmal
(b). atrial natriuretic hormone hipersecreţia
(c). #hipovolemie
(d). hipervolemie
(e). heavy intravenous fluid infusion
63. What is the cause of secondary hiperaldosteronismului?
a. essential arterial #hipertensiune

(b). hipervolemie
(c). paroxysmal
(d). heavy intravenous fluid infusion
(e). atrial natriuretic hormone hipersecreţia
a. liver ischemia
(b). hyperemia of the kidneys
(c). kidney #ischemia
(d). hyperemia of the liver
(e). cerebral ischemia
65. What are the causes of secondary hiperaldosteronismului?
a. angiotesinogena I
(b). #hipersecreţia Renin
(c). #hipersecreţia angiotesinogena II
(d). hipersecreţia angiotensin converting enzyme
(e). atrial natriuretic hormone hipersecreţia
a. tumaoare angiotesinogenă I-secreting

(b). tumaoare angiotesinogenă II-secreting
(c). tumaoare secretory enzyme angiotensin-converting
(d). tumaoare atrial natriuretic hormone-secreting
(e). #tumaoare Renin-secreting
a. insufficiency angiotesinogenei I
(b). angiotesinogenei on failure
(c). insufficiency of angiotensin converting enzyme
(d). atrial natriuretic hormone insufficiency
(e). liver #insuficienţa
a. #hipersecreţia of ACTH
(b). hipersecreţia of glucocorticosteroizi
(c). primary hipersecreţia of aldosterone
(d). hiposecreţia of ACTH
(e). hiposecreţie of glucocorticosteroizi
69. What is hiperaldosteronismul?
a. hiponatriemie
(b). #hipernatriemie
(c). hyperkalaemia
(d). hipercalciemie
(e). hipocalciemie
a. intravascular dehydration
(b). interstitial dehydration
(c). #hipokaliemie
(d). hipercalciemie
(e). hipocalciemie

a. intravascular dehydration
(b). interstitial dehydration
(c). interstitial #hiperhidratare
(d). hyperkalaemia
(e). hipocalciemie
a. peripheral vascular resistance #creşterea

(b). low blood pressure
(c). arteriolar hipotonusul
(d). desensitization of catecholamine vascular myocyte
(e). dilating peripheral blood vessels
a. increase peripheral vascular resistance

(e). #hipokaliemie
a. peripheral vascular resistance #creşterea

(e). #hipernatriemie

(e). interstitial #hiperhidratare
76. What is hipoaldosteronismul?
a. #hiponatriemie
(b). hipernatriemie
(c). hypokalemia
(d). hipercalciemie
(e). hipocalciemie
a. hipernatriemie
(b). #hiperkaliemie
(c). hypokalemia
(d). hipercalciemie
(e). hipocalciemie
a. Remove excessive potassium in the urine

(b). excessive muscle function #eliminarea with urine
(c). oliguria
(d). hipernatriemie
(e). hypokalemia

(b). #hipotensiune pressure
(c). Arteriolar Hipertonusul
(d). hipersensibilizarea vascular myocyte versus Catecholamines
(e). peripheral vessel spasm
a. hipertonusul skeletal muscles

(b). muscle #astenie
(c). increased excitability of nerve
(d). hiperreflexie
(e). skeletal muscle spasm
(d). #hiponatriemie
(d). #hiperkaliemie
(d). excessive muscle function #eliminarea with urine
(d). muscle #astenie
85. What is the importance of glucocorticosteroizilor in biological stress reaction?
a. reduces the body's resistance to stressor factors

(b). # increase the body's resistance to stressor factors
(c). #stimulează the catabolic processes
(d). stimulates anabolic processes
(e). inhibits the catabolic processes

a. #creşte blood pressure
(b). artterială pressure decreases
(c). #creşte cardiac output
(d). #creşte brain infusion
(e). infusion decreases skeletal muscles

a. synthesis of #creşte AS cardiotrope positive effects
(b). decreases the synthesis of the cardiotrope negative effects
(c). recapture as sinapsele #inhibă adrenergic cardiotrope positive effects
(d). #inhibă MAO activity and amplify the effects of adrenergic
(e). stimulates adrenergic effects and lessens MAO

a. synthesis of #creşte AS cardiotrope positive effects
(b). decreases the synthesis of the cardiotrope negative effects
(c). recapture as sinapsele #inhibă adrenergic cardiotrope positive effects
(d). #inhibă activity of COMT and amplifies the effects of adrenergic
(e). stimulates adrenergic effects and lessens MAO
89. What are the metabolic effects of glucocorticoizilor?
a. hypoglycemia
(b). #hiperglicemia
(c). #gluconeogeneza
(d). hipoproteinemia
(e). hipoaminoacidemia
a. glicogenogeneza
(b). proteosinteaa
(c). hiperproteinemia
(d). negative nitrogen #bilanţ
(e). positive nitrogen balance
a. #Glicogenoliza
(b). glicogenogeneza
(c). proteosinteaa
(d). #hiperglicemia
(e). positive nitrogen balance

a. glicogenogeneza
(b). proteosinteza
(e). #proteoliza
a. glicogenogeneza
(b). proteosinteza
(e). #inhibiţia proteosintezei
94. What are the metabolic organotrope of glucocorticoizilor?
a. myocardial atrophy
(b). atrophy of adipose tissue
(c). atrophy of nervous tissue
(d). atrophy of the skin
(e). connective tissue #atrofia
95. What are the effects of the organotrope of glucocorticoizilor?
(c). atrophy of nervous tissue
(d). atrophy of the skin
(e). thymus #atrofia
96. What are the effects of the organotrope of glucocorticoizilor?

(c). #atrofia skeletal muscles
(d). atrophy of nervous tissue
(e). atrophy of the skin
97. What is the importance of biological ontogenesis in antenatal

glucocorticosteroizilor of the lungs?
a. stimulates the development of bronhial tree
(b). stimulates alveolocitelor proliferation and synthesis of surfactant
(c). #stimulează alveolocitelor on proliferation and synthesis of surfactant
(d). stimulates proliferation of alveolar macrofagilor
(e). stimulate the development of local immunity
98. What is the importance of biological glucocorticosteroizilor in the ontogenesis of

antenatal thyroid?
a. stimulates the synthesis of thyroid hormones

(b). stimulates the thyroid iodine capture the foetus
(c). capture boosts maternal thyroid hormone
(d). enzymes in the synthesis of thyroid #contribuie hormonogenetice
(e). stimulates the proliferation of fetal thyroid
99. What is the importance of biological ontogenesis in antenatal
glucocorticosteroizilor of the digestive tract?
a. stimulates the proliferation of intestinal mucosa

(b). #stimulează synthesis of digestive enzymes
(c). stimulate the development of local immunity
(d). stimulates the development of the autonomic nervous system
(e). stimulates the formation of intestinal barrier
100. What is the importance of biological glucocorticosteroizilor in the ontogenesis of
antenatal?
a. #stimulează enzymes that synthesizes rhodopsin
(b). rezelei nerve stimulates the development of the retina
(c). stimulates the development of optical media
(d). stimulates the formation of the blood-ophthalmic
(e). stimulates the development of neuromuscular terminaţiunilor eye
101. What is the role of hormones in glucocorticosteroizi inflammatory reaction?
a. directly inhibits cytokines proinflammatory genes

(b). #inhibă NF-kB and proinflammatory cytokines genes indirectly
(c). the anti-inflammatory cytokine genes directly
(d). Activate NF-kB and proinflammatory cytokines genes indirectly
(e). nuclear receptors to inhibit NF-kB
102. What is the role of glucocorticosteroizi in the reaction inflammatory hormones?
f. stimulates inflammatory reaction causing inflammation hiperergică

g. inhibits inflammatory reaction causing inflammation hipoergică
h. #modulează inflammatory response while maintaining normoergică
inflammation
(i). intensifies the immune response and reduces inflammatory reaction
j. inhibit immune response but intensify inflammatory reaction
102. How hormones affect vascular reactions in glucocorticosteroizi on the
inflammatory reaction?
a. enables NO-aldosterone synthase, increase the concentration of NO and

dilates tiny arterioles
(b). inhibits the aldosterone synthase, dropping NO-concentration of NO and
dilates tiny arterioles
(c). #inhibă NO-aldosterone synthase, decrease the concentration of NO and
spasmează tiny arterioles
(d). decreases vascular endothelial reactivity to NO and spasmează tiny
arterioles
(e). increase the reactivity of NO and endothelium spasmează tiny arterioles
103. How do hormones influence on the process of exsudare glucocorticosteroizi in
inflammatory reaction?
a. increase hydrostatic pressure in the capillaries and helps to exsudare

(b). oncotică pressure in capillaries weaken and contribute to exsudare
(c). capillary permeability in capillaries grow and contribute to exsudare
(d). capillary permeability in capillaries weaken and contribute to exsudare
(e). capillary permeability and dimimnuează #scad exsudarea
104. How hormones affect glucocorticosteroizion the process of emigration of
inflammatory reaction in leucocietelor?
a. increase the concentration of leukocytes in the blood and contributes to

out-migration
(b). #scad concentration of leukocytes in the blood and reduces migration
(c). increase the strength of the integrine selectine and emigration
(d). decrease the concentration of selectine and integrins and emigration
(e). #scad concentration of integrins and retained and selectine emigration
105. What is pathogenesis of tertiary hipertiroidismului?
a. producentă thyroid tumor of thyroid hormones

(b). tumor of the pituitary gland hormone thyrotropin, producentă
(c). #hiperproducţia of tiroliberină
(d). excessive intake of iodine
(e). dietary iodine deficiency
106. What is pathogenesis of secondary hipertiroidismului?

a. producentă thyroid tumor of thyroid hormones
(b). #tumoare of hypophysis hormone thyrotropin, producentă
(c). hiperproducţia of tiroliberină
107. What is pathogenesis primary hipertiroidismului?
a. #tumoarea thyroid producentă thyroid hormones

(b). tumor of the pituitary gland hormone thyrotropin, producentă
(c). hiperproducţia of tiroliberină
108. How doI change the concentration of hormones in the blood in a tertiary
hyperthyroidism?
a. tiroliberina, thyrotropin, underperforming thyroid hormones

(b). high tiroliberina, low thyroid hormones, thyrotropin reared
(c). tiroliberina low, increased thyroid hormones, thyrotropin reared
(d). tiroliberina low, low thyroid hormones, thyrotropin reared
(e). #tiroliberina, thyroid hormones, thyrotropin reared
109. How doI change the concentration of hormones in the blood secondary
hyperthyroidism?

(c). #tiroliberina low, increased thyroid hormones, thyrotropin reared
(e). tiroliberina, thyroid hormones, thyrotropin reared
110. How doI change the concentration of hormones in the blood in primary
hyperthyroidism?

(c). tiroliberina low, increased thyroid hormones, thyrotropin reared
(d). #tiroliberina low, low thyroid hormones, thyrotropin reared
(e). tiroliberina, thyroid hormones, thyrotropin reared
111. What are the causes of tertiary hypothyroidism?

a. pituitary disorders
(b). inflammation of the thyroid gland
(c). hypothalamic #afecţiuni
(d). iodine deficiency in food ration
(e). thyroid removal
112. What are the causes of hypothyroidism secondary?

a. pituitary #afecţiuni
(b). diseases of the thyroid gland
(c). hypothalamic disorders
(d). iodine deficiency in food ration
(e). thyroid removal
113. What causes primary hipotiroidismulu?
a. pituitary disorders
(b). hypothalamic disorders
(c). tirotropinei failure
(d). tiroliberinei failure
(e). pathological in #procese thyroid gland
114. How do I change the concentration of hormones in the blood in secondary

hiptiroidismul?
a. tiroliberina low, low thyroid hormones, thyrotropin waxes

(b). tiroliberina low, thyrotropin, thyroid hormones scăuzţi
(c). tiroliberina, thyrotropin, underperforming thyroid hormones
(e). high #tiroliberina, low thyroid hormones, thyrotropin waxes
115. How do I change the concentration of hormones in the blood in primary

hypothyroidism?
a. tiroliberina low, low thyroid hormones, thyrotropin waxes
(b). tiroliberina low, thyrotropin, thyroid hormones scăuzţi
(c). #tiroliberina, thyrotropin, underperforming thyroid hormones
(e). high tiroliberina, low thyroid hormones, thyrotropin waxes
116. How to change the energy metabolism in hypothyroidism?

a. oxidative processes #diminuarea
(b). #scăderea basal metabolism
(c). increase oxygen consumption
(d). #scăderea body temperature
(e). Increases basal metabolism
117. How do I change thermoregulation in hypothyroidism?
a. Thermogenesis creeşte; body temperature increases thermolysis; constant

(b). Increases Thermogenesis, body temperature falls; thermolysis increases
(c). #Termogeneza decreases the thermolysis temperature increase;; body
drops
(d). Thermogenesis decreases, the temperature drops, thermolysis body
grows
(e). Thermogenesis, thermolysis and body temperature does not change
118. How do I change the body's adaptation with hypothyroidism at room temperature?
a. High temperature Intolerance and predisposition to hyperthermia
(b). High and low temperature Intolerance
(c). #Intoleranţa low temperatures and predisposition to hypothermia
(d). Înallte temperature Tolerance and intolerance low temperatures
(e). High temperatures, but Intolerance intolerance low temperatures
f. Low and high temperature Tolerance
119. How do I change the metabolism of lipid in hypothyroidism?

a. #hipercolesterolemie with with fractions VLDL, LDL and predisposition
to ateromatoză
(b). hypercholesterolemia with HDL without ateromatoză
(c). hypercholesterolemia with fractions VLDL, LDL and HDL
(d). hypercholesterolemia cholesterol catabolism picks up
(e). #hipercolesterolemie with the decrease in cholesterol metabolism
120. What are the effects of heart in hypothyroidism?
a. tachycardia with hypertension
(b). #bradicardie with hypotension
(c). atrial fibrillation with tachycardia
(d). tachycardia with atrioventricular block
(e). bradycardia with atrial fibrillation
121. What are the effects of heart in hyperthyroidism?

a. #tahicardie with hypertension
(b). bradycardia with hypotension
(c). atrial fibrillation with tachycardia
(d). tachycardia with atrioventricular block
(e). bradycardia with atrial fibrillation
The endocrine pancreas

122. How do I change diuresis in type I diabetes?
a. polyuria with izostenurie

(b). polyuria with hipostenurie
(c). #poliurie with hiperstenurie
(d). oliguria with hiperstenurie
(e). oliguria with hipostenurie
123. What is pathogenesis of poliuriei in type I diabetes?
a. incomplete reabsorption of primary urine potassium

(b). incomppletă reabsorption of urea in the urine of primary
(c). incomplete reabsorption of urine ketone body primary corpora
(d). #reabsorbţia incomplete primary urine glucose
(e). incomplete reabsorption of urine proteins in primary
124. What is the cause of hiperstenuriei in type I diabetes?
a. The presence in urine of ketone body coprpilor
(b). #prezenţa glucose in urine
(c). high concentration of urea in the urine
(d). the presence of protein in urine
(e). the presence in the urine uric acid
125. What is the cause of polidipsiei in type I diabetes?
a. Hipovolemia with hiponatriemie

(b). Hipovolemia with hyperkalaemia
(c). Hipovolemia with hiprkaliemie
(d). Hipovolemia with hipercetonemie
(e). # Hipovolemia with hipernatriemie
126. What is the cause of increased appetite in type I diabetes?
a. hypoglycemia
(b). hyperglycemia
(c). Hyperlipidemia
(d). glucagon
(e). catecolaminele
f. #leptina
127. How to change body mass in type I diabetes?
a. increase due to muscle hypertrophy
(b). increases by increasing body fat mass
(c). increase water retention in the body with swelling
(d). dehydrating the body drops
(e). #scade by decreasing body fat mass
128. How to change your metabolism in type I diabetes?
a. Reduces catabolism by insufficient insulin

(b). #Diminuează anabolismul by insufficiency of insulin
(c). Reduces catabolism by surplus glucocorticosteroizi
(d). Anablismul intensifies the glucagonului surplus
(e). Anablismul intensifies by catecholamine excess

(b). #Se intensifies the catabolism of glucocorticosteroizi surplus

(b). #Se enhances catabolism by excess Catecholamines

(b). #Se enhances the glucagon excess catabolism
132. How do I change the mass of skeletal muscle in type I diabetes?

a. increase due to muscle hypertrophy
(b). increases by increasing muscle mass and body fat
(c). increase water retention in the muscles
(d). dehydrating muscles decreases
(e). decreases in muscle atrophy
133. What cells are equipped with insulindependente Glut receptors?
a. striated #miocitul
(b). neuron
(c). renal epiteliocitul
(d). enterocitul
(e). hepatocitul
a. #adipocitul
(b). neuron
(d). enterocitul
(e). hepatocitul
a. #leucocitele
(b). neuron
(d). enterocitul
(e). hepatocitul
136. What conditions ensure glucose utilization by insulin in absence of neuron?
1. #glucokinaza insulinindependentă
2. #receptorii insulinindependenţi Glut
3. fosforilaza insulinindependentă
4. insulinindependentă phosphatase
5. Krebs Cycle insulinindependent
137. In what cell hexokinaza is insulindependentă?

a. leukocytes
(b). neuron
(d). enterocitul
(e). #hepatocitul
138. What is pathogenesis of hyperglycemia in type I diabetes?
a. intense mobilization of glucose from glycogen fiactului

(b). intense mobilization of glucose from glycogen striated muscles
(c). gluconeogeneza of fatty acids
(d). gluconeogeneza of amino acids
(e). excessive ingestion of carbohydrates with foods
a. #Glicogenoliza caused by glucagon in hepatocytes

(c). gluconeogeneza of fatty acids caused by glucocorticosteroizi
(d). Inhibition of glucose proteosintezei in the absence of insulin
(e). Inability of the kidneys to remove excess glucose in the absence of
insulin
a. #Glicogenoliza in hepatocytes induced by Catecholamines

insulin
a. #Gluconeogeneza of amino acids caused by glucocorticosteroizi

insulin
a. #Inibiţia glicogenogenezei in the absence of insulin

insulin
a. #Inhibiţia lipogenezei of grşi acids in the absence of insulin

insulin
a. #imposibiltatea the use of glucose in the muscles striated in the absence of

insulin
insulin
145. What is the cause of muscle atrophy in type I diabetes?

a. neasimilarea glucose in the absence of insulin
(b). neasimilarea fatty acids in the absence of insulin
(c). mioliza by the action of glucagon excess
(d). anabolic effects of insulin #lipsa
(e). patients ' hypodynamia
146. What is the cause of muscle atrophy in type I diabetes?
a. neasimilarea glucose in the absence of insulin

(b). neasimilarea fatty acids in the absence of insulin
(c). mioliza caused by glucagon
(d). #mioliza caused by glucocorticosteroizi
(e). patients ' hypodynamia
147. What is the cause of erectile dysfunction in men in type I diabetes?
a. corpora cavernoşi atrophy in the absence of insulin

(b). reducing sympathetic influences on the arterioles corpora cavernoşi
(c). amplification of parasympathicus influences on vessels cavernoşi
corpora
(d). #ateroscleroza pudende artery
(e). #hipoandrogenia caused by corticosteroids
148. What is the cause of coronary insufficiency in type I diabetes?
a. glucose neasimilarea by the miocardiocit in the absence of insulin

(b). neasimilareai of the miocardiocit of the fatty acids in the absence of
insulin
(c). coronary artery #ateroscleroza
(d). amplification of beta-adrenergic influences on coronary vessels
(e). parasympathicus influences on the amplification of myocardium
149. What is the cause of Visual disorders in type I diabetes?
a. neasimilarea of glucose by the cells of the retina in the absence of insulin

(b). neasimilarea fatty acids by the cells of the retina in the absence of
insulin
(c). atherosclerosis of arteries of the retina
(d). microvaselor retina #microangiopatia
(e). opacificarea vitreous body
150. What causes predisposition of patients with type I diabetes at piogene infection?
a. type humoral immunodeficiency

(b). type cellular immunodeficiency
(c). complement deficiency
(d). the shortage of phagocyte
(e). microbicides to fagociţilor activity #diminuarea
151. Thatis causing a reduction in the activity of microbicides fagociţilor in patients

with type I diabetes?
a. glucagon inhibits free radical production in the fagocitului cytoplasm

(b). #lipsa insulin inhibits the production of free radicals in the fagocitului
cytoplasm
(c). Lysosomal enzyme activity inhibits glucagon to fagocitului
(d). lack of Lysosomal enzymes inactivate insulin fagocitului
(e). glucocorticosteroizii-inducing apoptosis of neutrophil leukocytes
152. What is the cause of slow wound regeneration in patients with type I diabetes?
a. glucocorticosteroizii inhibits proteosinteza

(b). proteosinteza inhibits glucagon
(c). #în lack of insulin to inhibit proteosinteza
(d). the lack of growth factors
(e). amino acid deficiency
153. How do I change lipidograma in patients with type I diabetes
a. #creşte concentration of VLDL

(b). #creşte LDL concentration
(c). decreases the concentration of chilomicronilor on nemâncate
(d). decreases the concentration of VLDL
(e). #creşte the concentration of free fatty acids
154. How to change the acid-base balance in patients with type I diabetes?
a. metabolic #acidoză
(b). gaseous acidosis
(c). excretory acidosis
(d). exogenous acidosis
(e). lactoacidoză
155. Accumulation of acids which cause acidosis in patients with type I diabetes?
a. lactic acid
(b). pyruvic acid
(c). #acidul acetoacetic
(d). #acidul beta-hidroxibutiric
(e). acetic acid
156. How do I change the protein metabolism in type I diabetes?
a. anabolismul prevails over the protein catabolism

(b). protein catabolism to anabolism #predomină
(c). positive nitrogen balance
(d). intensifies the synthesis of nucleoproteidelor
(e). intensifies the synthesis of apolipoproteins
157. That is a negative nitrogen balance of pathogenesis in type I diabetes?
a. insulin #deficitul
(b). the excess glucagon
(c). excess of Catecholamines
(d). #surplusul of glucocorticosteroizi
(e). Deficiency of glucagon
158. What is the mechanism of glucozuriei in patients with type I diabetes?

a. in the absence of insulin ihibă glucose reabsorption is the primary urine
(b). the excess glucagon glucose reabsorption of urine inhibits primary
(c). renal glucose reabsorption impairs microangiopatia from primary urine
(d). #concentraţia of glucose in urine exceeds the capacities of primary
reabsorption of renal epithelium
(e). Hyperglycemia leads to excessive filtraţia of glucose in the urine of
primary
159. At what level of blood sugar occurs glucozuria in patients with type I diabetes?
a. in the absence of insulin at any concentration of glucose in the blood

(b). the excess glucagon at any concentration of glucose in the blood
(c). #la concentration of more than 10 mMol/L
(d). at concenztraţi over 6 mMol/L
(e). the concentration of over 20 mMol/L
160. What is the mechanism of albuminuriei in patients with type I diabetes?
a. in the absence of insulin to inhibit reabsorption albumins from primary

urine
(b). the excess glucagon intensifies Glomerular filtraţia of albumins
(c). #creşterea permeability of Glomerular basement membrane of the
capillaries
(d). increased permeability of the renal tubule basement membrane
(e). disintegration of renal epiteliocitelor
3. PATHOPHYSIOLOGY of BLOOD (77)
1. What are the parameters normovolemiei normocitemice?

a. the total volume of blood 7% of body weight; erythrocyte count12/l-7.10;
56% hematocrit
b. the total amount of blood 5% of body weight; erythrocyte count12to 3.10;
32% hematocrit;
c. the total volume of blood 7% of body weight; erythrocyte count12to 3.10;
32% hematocrit
d. the total volume of blood by 9% of body weight; erythrocyte count12/l-7.10;
56% hematocrit
e. * the total volume of blood 7% of body weight; erythrocyte count12to 5.10;
42% hematocrit
2. under what conditions is found hipovolemia simple?

a. more than 30-40 minutes after acute acute hemorrhage
b. over 72 hours after acute hemorrhage
c. in the shock combustitional
d. in hyperthermia
e. in iptermie
3. What are the parameters for long oligocitemice?

a. the total volume of blood 5% of body weight; the number of erythrocytes 5.1012/L;
42% hematocrit
b. the total amount of blood 7% of body weight; erythrocyte count12/l-7.10;
56% hematocrit
c. * the total volume of blood 5% of body weight; erythrocyte count12to 3.10;
32% hematocrit;
d. the total volume of blood 7% of body weight; erythrocyte count12to 3.10;
32% hematocrit
e. the total volume of blood 5% of body weight; erythrocyte count12/l-7.10;
56% hematocrit
4. under what conditions is found hipovolemia oligocitemică?

a. inthe first few minutes after hemorrhage in acute
b. * more than 24 hours after hemorrhage acute
c. in eritremie
d. in hyperthermia
e. in hiptermie
5. What are the parameters for long policitemice?

a. the total volume of blood 5% of body weight; erythrocyte count12to 5.10;
42% hematocrit
56% hematocrit
c. * the total volume of blood 5% of body weight; erythrocyte count12/l-7.10;
the hematocrit 56%;
32% hematocrit
(e). the total volume of blood, 9% of the body weight; erythrocyte count12/l-7.10;
56% hematocrit
6. In what state it is found hipovolemia policitemică?

a. * hyperosmolar dehydration
b. * in combustion
c. in eritremie
d. in anemia
e. * dehydration izoosmolară
7. What are the parameters hipervolemiei oligocitemice?

42% hematocrit
56% hematocrit
32% hematocrit;
32% hematocrit
e. total blood volume 9% of body weight; erythrocyte count12to 3.10;
32% hematocrit
8 . In what States is found hipervolemia oligocitemică ?

a. massive infusions of the isotonic cleaners
b. in excessive blood transfusions
c. in transfuzi of cell nasă
d. in polidipsia in diabetes mellitus
e. in polidipsia in diabetulinsipid
9. What are the parameters hipervolemiei policitemice?

42% hematocrit
56% hematocrit
32% hematocrit;
32% hematocrit
e. total blood volume 9% of body weight; erythrocyte count12/l-7.10;
56% hematocrit
10. under what conditions is found hipervolemia policitemică ?

a. eritremie *
b. in renal failure
c. in excessive blood transfusions
d. in polidipsia in diabetes mellitus
e. in polidipsia in Diabetes Insipidus
11. What are the signs of the disorder in the eritroblastică cellular diferenţieirii?
a. increasing the number of proeritroblaşti, eritroblaşti, normoblaşti and reticulocytes in
Red marrow
b. increase the number of normoblaşti and in peripheral blood reticulocytes
c. increasing the number of eritroblaşti, normoblaşti and in peripheral blood reticulocytes
d. * increase proeritroblaşti, eritroblaşti while lowering
the number of reticulocytes and normoblaşti in the Red marrow
e. increase the number of eritroblaşti at the same time decreasing the number of
normoblaşti and in peripheral blood reticulocytes
12. What are the changes in the Red marrow hiperproliferarea mielogramei?
a. * increasing the number of eritroblaşti
(b). * increasing the number of normoblaşti
(c). * increasing the number of reticulociţi
(d). substitution with fat
(e). * expansia red marrow
13. What are modificţrile hiperproliferarea the Red marrow hemogram?

a. increasing the number of eritroblaşti
(b). * increasing the number of normoblaşti
(c). * increasing the number of reticulociţi
(d). eritrocitoză with neeficiente hemoconcentraţie, intensification of erythropoiesis
(e). eritrocitoză with hemodiluţie
14. What are the signs of hipocromiei?

a. * the content of hemoglobin in an erythrocyte under pg 29
(b). the content of hemoglobin in an erythrocyte below 40 pg
(c). * chromatic given less than 0,8
(d). * erythrocyte sedimentation anulară form
(e). * average hemoglobin concentration in erythrocyte of less than 33%
15. What is one of the signs of hipocromiei?
f. * the content of hemoglobin in an erythrocyte under pg 29
g. the content of hemoglobin in an erythrocyte 40 pg
h. chromatic 0.9-1.1 given
(i). eliptoidă form anulară erythrocyte sedimentation
j. the average hemoglobin concentration in erythrocyte 33%
16. What are the signs of hipocromiei?

k. the content of hemoglobin in an erythrocyte pg 29
l. the content of hemoglobin in an erythrocyte 40 pg
m. * chromatic given less than 0,8
b. form eliptoidă erythrocyte sedimentation
it. the average hemoglobin concentration in erythrocyte 33%
p. the content of hemoglobin in an erythrocyte pg 29
q. the content of hemoglobin in an erythrocyte 40 pg
r. chromatic 0.9-1.1 given
s. * erythrocyte sedimentation anulară form
t. the average hemoglobin concentration in erythrocyte 33%

u. the content of hemoglobin in an erythrocyte pg 29
v. the content of hemoglobin in an erythrocyte 40 pg
w. chromatic 0.9-1.1 given
x. form eliptoidă erythrocyte sedimentation
y. the average hemoglobin concentration in erythrocyte under 33%
19. What is one of the signs of hipercromiei?

a. * the content of hemoglobin in an erythrocyte over 30 pg
(b). the content of hemoglobin in an erythrocyte equal to 29 pg
(c). * chromatic given greater than 1,1
(d). given the chromatic equal to 1
(e). the average hemoglobin concentration in erythrocyte of more than 33%
20. What are the signs of macrocitozei?

a. the average diameter of greater than 8 μ
b. * the average volume of erythrocytes larger than 90 fl
c. * the average thickness of greater than 4 µ
d. elipsoidă form of erythrocytes
e. the average hemoglobin concentration in erythrocyte of more than 33%
21. What is one of the signs of macrocitozei?
a. the average diameter of greater than 8 μ
b. average volume of erythrocytes 90 fl
c. the average thickness of 4 μ
a. the average diameter of 8 μ
b. * the average volume of erythrocytes larger than 90 fl
c. the average thickness of 4 μ
a. the average diameter of 8 μ
b. average volume of erythrocytes 90 fl
c. * the average thickness of greater than 4 µ
24. What are the signs of primary eritrocitozei (eritremiei)?
a. granulocitoză *
b. erythrocyte count greater than 5.1012/L
c. * reticulocytes count greater than 2.5%
d * trombocitoză
e. the number of reticulocytes below 0,5%
2 22 . What are the signs of primary eritrocitozei (eritremiei)?
a. granulocitoză *
c. * reticulocytes count greater than 2.5%
d * trombocitoză
e. the number of reticulocytes below 0,5%
25. In what state it is found isthe primary ritrocitoza ?
a. in anemia
b. in vomit incoercibilă
c. in renal diseases
d. in hypoxies
e. *in eritremie
26. What are the signs of secondary eritrocitozei absolute?

a. content of hemoglobin of more than 160 g/L
c. * reticulocytes count greater than 0,5%
d. the total volume of blood under 7% of body weight
e. * hematocrit greater than 45%
27. In what state is established it'ssecondary absolute ritrocitoza?

а. * residents of regions from coat-
b. vomiting in pregnant women with incoercibilă
c. the dehydrated patients
d. *in patients with chronic respiratory diseases
е. * in chronic hypoxia
а. * residents of regions from coat-
d. in patients with acute respiratory diseases
е. in acute hypoxia
а. the inhabitants of the Mediterranean regions
d. *in patients with chronic respiratory diseases
е. in acute hypoxia
а. the inhabitants of the Mediterranean regions
d. in patients with acute respiratory diseases
е. * in chronic hypoxia
31. What are the signs of the relative secondary eritrocitozei?

a. content of hemoglobin of more than 160 g/L
c. the number of reticulocytes = 0,5%
d. hiperproliferarea eritrocitare series of Red marrow
e. * the total volume of blood under 7% of body weight
32. In what state the relative secondary eritrocitoza?

а . * in arşilor disease
b. * in vomit incoercibilă
c. * deshidratatrea body
d. in chronic hypoxia
e. in eritremii
33. In what state the relative secondaryeritrocitoza?
а . * in arşilor disease
b. in iron deficiency anemia
c. anemia megaloblastică
e. in eritremii
а . b. in iron deficiency anemia
b. * in vomit incoercibilă
e. in eritremii
а . b. in iron deficiency anemia
c. * deshidratatrea body
e. in eritremii
35. what process is normally in hypo-aplastic anemia?

a. differentiation of all cells, mainly bone marrow eritroblastice series
(b) * the proliferation of bone marrow cells mostly all of the series eritroblastice.
c. hemoglobin synthesis
d. eritrodiereza
e. maturaţia erythrocytes
36. How do I change the blood count anemia hypo-aplactică?

a. Leukocytosis neutrofilă.
b. Drepanocitoză.
c. Megalocitoză.
d. Trombocitoză.
e. * Pancitopenia.
37. What are pancitopenia?

a. micşoraea the total number of erythrocytes in the peripheral singele
b. decreasing agranulocite in peripheral singele
c. increase in the number of platelets in peripheral singele
d. * reduction in the number of granulocytes, erythrocytes and platelets in peripheral singele
e. increasing the figurative elements all in peripheral singele
38. what processes are normally in hemolytic anemia?

a. proliferation of eritroblastice series
b. differentiation of series eritroblastice
d * eritrodiereza
39. what is one of the signs of intracellular hemolizei?
a. the presence of hemoglobin in the blood plasma
(b). lowering the amount of haptoglobină in blood plasma
(c). hemoglobinuria
(d). * hyperbilirubinemia with free bilirubin (indirect)
(e). hyperbilirubinemia with conjugated (direct) dilirubina
40. That is one of the signs of intracellular hemolizei?

f. the presence of hemoglobin in the blood plasma
g. lowering the amount of haptoglobină in blood plasma
h. #splenomegalie
(i). * hyperbilirubinemia with free bilirubin (indirect)
j. hyperbilirubinemia with conjugated (direct) dilirubina
41. That is one of the signs of severe intravasculare hemolizei?

a. * the presence of hemoglobin in the blood plasma
(b). * lowering the amount of haptoglobină in blood plasma
(c). * hemoglobinuria
(d). * hyperbilirubinemia with free bilirubin (indirect)
(e). hyperbilirubinemia with conjugated (direct) dilirubina
42. What are the signs of severe intravasculare hemolizei?
f. * the presence of hemoglobin in the blood plasma
g. Ceşterea amount of haptoglobină in blood plasma
h. * hemoglobinuria
(i). Cncentraţie normal bilirubin levels in the blood
j. hyperbilirubinemia with conjugated (direct) dilirubina
43 . What are the signs of severe intravasculare hemolizei?
k. * the presence of hemoglobin in the blood plasma
l. Ceşterea amount of haptoglobină in blood plasma
m. * lowering the amount of haptoglobină in blood plasma
b. * hemoglobinuria
it. hyperbilirubinemia with conjugated (direct) dilirubina
44 . What process is in iron deficiency anemia impairs?

a. proliferation of eritroblastice series
c. hemoglobin synthesis *
d. eritrodiereza
45. How do I change the blood count anemia iron deficiency?

a. Megalocitoză.
b. *Hipocromia erythrocytes
c. *Microcitoză
d *Anulocitoză.
e. Drepanocitoză
46. the anemia is found microcitoza ?

a. *Anemia fierodeficitară.
b. *hereditary Hemolytic Anemia (Minkowski-Chauffard disease).
c. posthemoragic Anemia, acute.
d. *posthemoragică chronic Anemia.
e. hypo-Aplastic Anemia
a. *Anemia fierodeficitară.
b. acquired Hemolytic Anemia
d. B12 deficient Anemia
a. B12 deficient Anemia
b. *hereditary Hemolytic Anemia (Minkowski-Chauffard disease).
d. b.Acquired Hemolytic Anemia
a. B12 deficient Anemia.
b. acquired Hemolytic Anemia
d. *posthemoragică chronic Anemia.
50. what processes are normally in anemia B12 -deficient?
the proliferation of series eritroblastice.
d * eritrodiereza
e. * maturaţia erythrocytes
51. How do I change the blood count anemia B-12deficient?

a. *Hipercromia erythrocytes
b *Megalocitoză
(c). *Thrombocytopenia
D *Cabot rings and Red corpuscles Jolli
e. Neutrofilie with nuclear diversion to the left.
52. the anemia is megaloblastic type erythropoiesis ?

a. -Thalassemia.
b. * Anemia folic acid deficiency
c. * Deficiency Anemia and vitamin B12 .
(d).Hypo-Aplastic Anemia
e. fierodeficitară Anemia.
53. What are the signs of absolute leucocitozei?
a. the number of leukocytes in the blood more than 10.109/L
b. * the increase in the number of leukocytes in blood
c. the number of leukocytes in the blood normal
d. presence of leukocytes in the blood non-differentiated
e. increasing the percentage of a decrease in the white blood cell
otherwise, percentage of leukocytes in leucogramă
54. What are the signs of the relative leucocitozei?

a. #numărul of leukocytes in the blood more than9/L 9.10
(b). increase in the number of leukocytes in blood
(c). * the number of leukocytes in the blood normal
(d). The presence of leukocytes in the blood non-differentiated
(e). * increasing the percentage of forms at the same time lowering the percentage
other forms of leukocytes in leucogramă
55. That leucocitoze may be considered physiological?

a. miogenă *
b. inflammation
c. infectioasă
d. food *
e. to newborns
56. what Leukocytosis estefiziologică?
a. physical
b. in inflammation
c. in infeţioase diseases
d. the curative inaniţia
e. in healthy people aged

physically rested.
b. b. in inflammation
d. postprandial *
e. in healthy people aged

physically rested.
b. b. in inflammation
d. the curative inaniţia
e. to newborns
59. What is the cause of neutrofiliei?

a. suprarenaliană failure
(b). allergic diseases
(c). * cocică infection
(d). parasitosis
(e). specific chronic infection
60 . The boi is founditeucocitoza neutrofilă?

a. *Furunculosis
(b).in pregnant women
c. * otitis purulent
d. viral diseases
e. * heart attack of myocardium
61. What is diverting nuclear "left"?

to. agranulocite increase in peripheral singele
(b). increase in the number of granulocytes in the peripheral singele
c. * increasing the number of immature neutrophils in peripheral singele
d. increasing numbers of mature neutrophils in peripheral singele
e. increase the number of neutrophils in peripheral hipersegmentate singele
62 . In what state is iteucocitoza neutrofilă hiperregenarativă?

a. the disease are
b. bone marrow aplaziа
c. benzene poisoning
d. * septicemia
e. suprarăcirea body
63. what States the Leukocytosis eozinofilă?
a. cocică infection
(b). * allergic diseases
(c). * parazitaree disease
(d). * chronic myeloid leukosis
e. * collagen disorder
64. In what state the Leukocytosis eozinofilă?

(e). cocică infection
f. * allergic diseases
g. chronic infectious diseases
h. acute myeloid leukosis
e. hereditary diseases
(i). cocică infection
j. chronic infectious diseases
k. acute myeloid leukosis
f. * parazitaree disease
g. cocică infection
h. chronic infectious diseases
(i). acute myeloid leukosis
j. * chronic myeloid leukosis
k. cocică infection
l. chronic infectious diseases e.
m. acute myeloid leukosis
f. * collagen disorder
68. what diseases are found limfocitoza?

a. suprarenaliană failure
(b). allergic diseases
(c). cocică infection
(d). parasitosis
(e). * specific chronic infection
69. what diseases are found limfocitoza?

a.tuberculosis
b. septicemia
c. thebronchial stmul
d. *chronic lymphoid leukosis
e. myocardial infarction
7 0. In what state the monocitoza?
a. during the convalescence of acute infections
b. *granulomatous inflammation
c. * infectioasă Mononucleosis
d. asthma
e. * Myeloid Metaplasia
71.. What is agranulocitoza?

a. increasing the number of lymphocytes and monocytes in peripheral singele
b *severe reduction or absence of granular leucocytes in peripheral singele
(c).increasing the number of leukocytes in peripheral agranulate singele
d. increasing the number of neutrophils in hipersegmentate perifericc singele
e. reduction punitive number of reticulocytes in the peripheral singele
72. In what state the agranulocytosis?

of aplastic anemia.
b. treatment with chemotherapy
c. parasitic diseases
d. allergic diseases
e. septicemia
73 . What processes it impairs leukosis in eritroblastică?

the proliferation of series eritroblastice.
d. eritrodiereza
e. * maturaţia erythrocytes
74. What are the signs of hematologic leukemia myeloid leukosis?

a. the number of leukocytes in excess of9 /L 50x10 associated with a
large numbers of cells in the peripheral blood blaste ....
b. WBC less than 50 x 109 /L associated with a number
cells in the blood of perigeric. blaste ...
c. WBC less than 6 x 109 /L associated with the presence of
by blaste ... cells in the peripheral blood.
d. sample rate is less than 6 WBC x 109 /L associated with the presence of
of cells in the Red marrow of blaste ... bones.
e. * invading blood cells non-differentiated leucocyte series
75. What are the signs of hematologic myeloid leukosis subleucemice?

a. the number of leukocytes in excess of 50 x 109 /L associated with a
considerable number of cells in the peripheral blood blaste ....
b. * WBC less than 50 x 109 /L associated with a
large numbers of cells in the blood of perigeric. blaste ...
d. sample rate is less than 6 WBC x 109 /L associated with the presence of
e. * invading blood cells with moderate non-differentiated leucocyte series
76. What are the signs of hematologic myeloid leukosis leucocitopenice?

a. the number of leukocytes in excess of 50 x 109 /L associated with a
considerable number of cells in the peripheral blood blaste ....
c. * WBC less than 5 x 109 /L associated with the presence of
d. sample rate of WBC less than 6 x 109 /L associated with the presence of
e. * the presence of cells in peripheral singele blaste ...
77. What are the signs of hematologic myeloid leukosis aleucemice?

a. the number of leukocytes in excess of 50 x 109 /L associated with a number
d. * WBC e 5-6 x 109 /L associated with the presence of
e. * lack of cells in peripheral singele blaste ...
4. pathophysiology of systemic circulation (68)
1. In what occurs with overuse of heart pathology resistance?

1. mitral Insufficiency
2. the insufficiency of aortic valve
* 3. High blood pressure
Tricuspid Insufficiency (4).
5. Anemia
2. In what siprasolicitarea heart disease occurs with volume?

1. Mitral stenosis
2. Mitral insufficiency *
3. Hipersecreţia adrenaline
4. Insufficiency of aortic valve *
5. Hipervolemia *
3. what diseases dismetabolică heart failure occurs?
1. Tricuspid insufficiency
2. Hypertensive disease
3. Myocardial infarction *
4. Myocarditis *
5. Aortic stenosis
4. What are the potential causes of heart failure right?

1. Hypertension in the small circulation *
2. Mitral insufficiency
3. Tricuspid insufficiency *
4. Aortic Coarctaţia
5. Emphysema lung *
5. What is the cause of heart failure right?
6. Hypertension in the small circulation *
8. Hypertension in high circlaţia
10. pulonar edema
6. What is the possible cause of heart failure right?
11. Hypertension in high circulation
13. Tricuspid insufficiency *
15. edemulpulmonar
7. What is the possible cause of heart failure right?
16. High blood circulation
18. hipovolemia
20. Emphysema lung *
8. What are the potential causes of left heart failure?

2. Aortic Coarctaţia *
3. Pulmonary emphysema
4. Hypertensive disease *
5. Pneumoscleroza
9. What is the cause of left heart failure?
7. hypertension in small circulation
9. hipovolemia
10. Pneumoscleroza
11. Tricuspidală failure
12. Aortic Coarctaţia *
14. Hipotensivă disease
15. Pneumoscleroza
16. Tricuspidală failure
17. pulmonary hypertension
19. Hypertensive disease *
20. Pneumoscleroza
12. What are the characteristic manifestations of left heart failure?

1. End-systolic volume discount *
2. * Tachycardia
3. Venous Stasis in the small circulation *
4. Shortness Of Breath *
5. Hepatomegalie
13. What are the characteristic manifestations for heart failure right?
1. Hepatomegalia *
2 Venous Stasis in the large circulation *
3. pulmonary edema
4. Venous Stasis in the small circulation
5. Ascites
14. What are the mechanisms of cardiac immediate compensatory heart diseases?
1. Bradycardia
2. * Tachycardia
3. hidrosalină Retention
4. myocardial Hypertrophy
5. Enhancing erythropoiesis
15. What is the compensation mechanism in the heart's pacemaker late?
1. Bradycardia
2. Paroxysmal
3. hidrosalină Retention
4. * myocardial Hypertrophy
5. Enhancing erythropoiesis
16. the compensatory mechanisms that are extracardiace immediate heart disease?
1. Redistribution of cardiac output with centralization movements *
2. Myocardial Hypertrophy
3. Increased parasympathetic nervous system tonus
4. Pulmonary Hiperventilaţia *
5. Increased erythropoiesis
17. the compensatory mechanisms that are late extracardiace in heart disease?
6. Redistribution of cardiac output with the centralization of
7. Myocardial Hypertrophy
8. Increased parasympathetic nervous system tonus
9. Pulmonary Hiperventilaţia
10. Increased erythropoiesis *
18. How is predominantly homeometrică hiperfuncţia of the myocardium?

1. By decreasing the amplitudinei myocardial contraction
2. Through the Frank-Starling mechanism
3. By increasing the amplitudinei myocardial contraction
4. By increasing myocardial tension *
5. With tachycardia
19. How is the predominant hiperfuncţia realizaeză heterometrică of the myocardium?

1. reduction of myocardial contraction amplitudinei
2. through the Frank-Starling mechanism *
3. by increasing myocardial contraction * amplitudinei
4. by increasing myocardial tension
5. by tachycardia
20. the heart is characteristic vices hiperfuncţia homeometrică?

1. The aortic stenosis *
2. Orifice of pulmonary trunk stenosis *
3. Valvulelor aortic insufficiency
4. Valvulelor mitral valve insufficiency
5. Valvulelor tricuspidale insufficiency
21. the heart deficiency is hiperfuncţia homeometrică feature?
6. The aortic stenosis *
7. The left atrioventricular orifice stenosis
22. the heart deficiency is hiperfuncţia homeometrică feature?
12. Orifice of pulmonary trunk stenosis *
23. the heart is characteristic vices hiperfuncţia heterometrică?

1. Mitral stenosis
2. The aortic stenosis
3. Valvulelor mitral valve insufficiency *
4. Insufficiency of aortic valve *
5. Orifice of pulmonary artery stenosis
24. For which is characteristic of heart deficiency hiperfuncţia heterometrică ?
6. Mitral stenosis
8. Valvulelor mitral valve insufficiency *
9. Right atrioventricular orifice stenosis
25. which is the characteristic heart defect hiperfuncţia heterometrică ?
11. Mitral stenosis
14. Aortic valve insufficiency *
26. How do I change the structure of myocardium hypertrophy in?

1. Increase the number of miofibrile
2. Increase the number of miofibrile with their decline
3. abundant growth of connective tissue
4. increase the volume of their miofibrilelor with decreasing
5. Increase the volume of their miofibrilelor but the number remains constant *
27. What are the mechanisms of functional cardiosclerozei of the myocardium and
hypertrophied limb?
1. Disturbing the energy of cardiomiocitelor *
2. relative hypoxia myocardium *
3. Increase IFS miocardioctelor intact *
4. Increase the pressure within the cavity of the pericardium
5. Decreases coronary perfusion pressure in
28. What is the cause of the relative hypoxia in the myocardium hypertrophied limb?
1. The spasm of coronary vessels
2. In Formation of atheromatous plates
3. Disruption of oxygen use
4. Energogenezei Malfunction
5. the relative failure of myocardium vasculaturii *
29. How do I change the volume and end-systolic volume of circulating blood in heart
failure?
1. End-systolic Volume shrinks, and circulating blood volume increase *
2. Both indices are increasing
3. End-systolic Volume increases, and the circulating blood volume decreases
4. Both indices shrinks
5. both indices are not changed
320. what causes chronic heart failure in hipervolemiei?
1. Venous Stasis
2. Mobilization of stored blood *
3. Hidrosalină Retention *
4. Increased Glomerular as urolithiasis
5. Increased erythropoiesis *
31. What are the consequences of venous stazei in circulatory insuficenţa?

1. hypoxia *
2. Oedema Formation *
3. Increasing the velocity of circulation of the blood
4. Decreasing processes of dissociation of oxihemoglobinei
5. Ketoacidosis
32. what anatomical regions Venous Stasis occurs in case of left ventricular failure?
1. In the facial region
2. In lower limbs
3. In the liver
4. In the brain
5. In the lungs *
33. What are the consequences of stazei vein in the liver?

1. hepatomegalia
2. hepatocyte death and substitution with connective tissue *
3. overuse of left ventricle
4. overuse of right ventricle
5. high blood portlă *
34. What are the causes of hypertension in liver cirrhosis portal hypertension?
1. insufficient colateralelor cava-cavale
2. Compression circuit sea vessels
3. colateralelor porto-insufficiency cavale
4. reducing the number of functional intrahepatice capillaries *
5. permiabilităţii Growth mezenteriale vessels
35. What are the consequences of portal hypertension hypertension?

1. Forming anastomoses porto-cavale *
2. * Ascites
3. Dilation of the veins of the lower oesophagus varicous *
4. Bleeding of veins of esophagus vericoase *
5. Forming anastomoses cava-cavale
36. What is the consequence of portal hypertension hypertension?
1. Forming anastomoses porto-cavale *
2. abdominal organ ischemia
3. Dilation of veins varicous feet
4. Bleed the hemorrhoidal veins
2. * Ascites
2. organeor abdominal ischemia
3. Dilation of the veins of the lower oesophagus varicous *
2. organeor abdominal ischemia
4. Bleeding of veins of esophagus vericoase *
40. In which Venous Stasis disease develops in the liver?

1. hypertensive Disease
2. arterial Hypotonia
3. the Hypovolemic
4. right ventricular Failure *
5. left ventricular Failure
41. In what case is form anastomoze porto-cavale?

2. in the case of portal hypertension *
3. the hypovolemic shock
4. hipervolemie
5. chronic arterial hypotonia
42. What are the factors of patogenetici cardiac oedema?

1. hiperseceţia Renin kidney and hipoperfuzia *
2. * Venous Stasis
3. hepatic and hipoalbuminemia *
4. arterial hypotension
5. hypoxia
43. What are the factors of patogenetici cardiac oedema?

6. * Venous Stasis
7. secondary hiperaldosteronismul *
8. hipervolemia *
10. hypoxia
44. What is one of the factors of patogenetici cardiac oedema?

11. hiperseceţia Renin kidney and hipoperfuzia *
13. hypoxia
45. That is one of the factors of patogenetici cardiac oedema?
16. * Venous Stasis
18. hypoxia
21. secondary hiperaldosteronismul *
23. hypoxia
26. hepatic and hipoalbuminemia *
28. hypoxia
48. That is one of the factors of patogenetici cardiac oedema?
31. hipervolemia *
33. hypoxia
49. What is the role of pathogenesis of kidney hipoperfuziei oedema?

1. kidney parenchyma edema
2. enabling device-juxta glomerulus *
3. kidney parenchyma ischemia
4. inflammation of the kidney parenchyma
5 arterial vessels in nefronului.
50. What is pathogenesis of secondary hiperaldosteronismului in circulatory insuficenţa?

1. hipersecreţia of aldosteronului
2. hiperreninemia *
3. degradation of aldosteronului by the insufficiency of liver *
4. reduction of renal excretion of aldosteronului
5. secreţa aldosteronului by the liver
15. how to change your metabolism in the myocardium in the initial phase of hypertrophy?
1. Reduction of oxidative processes
2. Reduction of glicolitice processes
3. Intense Use of ATP *
4. Increased use of oxygen *
5. Enhancement of protein synthesis *
52. How do I change in venous blood pressure and heart failure?

1. Venous blood pressure and increase
2. Blood pressure decreases, and the increase vein *
3. Arterial and venous Pressure does not change
4. And venous blood pressure decreases
5. blood pressure increases and decreases venous
53. How do I change the volume endsistolic volume and the end-systolic heart failure?
1. End-systolic Volume increases, and the volume is micşoreză endsistolic
2. Both indices shrinks
3. End-systolic Volume shrinks, the volume remains unchanged endsistolic
4. Both indices are increasing
5. End-systolic Volume shrinks, and the volume increase * endsistolic
54. how intracardiace conduction disturbance manifests?

1. atrioventricular block *
2. bradycardia sinuzală
3. sinuzală tachycardia
4. extrasistolie
5. Ventricular fibrillation
55. For what disorders is bradycardia sinuzală feature?
1. Pulmonary edema
2. Thyrotoxicosis
3. Mechanical Jaundice *
4. Pulmonary Emphysema
5. Meningitis *
57. what extrasistolie is the full compensatory pause feature?

1. Extrasistolie sinuzală
2. Atrial Extrasistolie
3. Extrasistolie atrioventriculară at the top
4. Ventricular Extrasistolie *
5. The average atrioventriculară Extrasistolie
58. What is manifested disturbance of the excitability of heart?
1. Bradycardia
2. Transverse complete Block
3. Longitudinal Block
4. Tachycardia
5. Extrasistolie *
61. what is disturbing heart also permits?

1. Atrioventricular block
2. Bradycardia sinizală *
3. Sinuzală * tachycardia
4. Extrasistolie
5. Atrial fibrillation
62. What are the bradicardiei causes sinuzale?

1. Vaso-constrictor Centre excitation
2. Activation of the sympathetic nervous system
3. Excitation of vagus nerve center *
4. Hisse beam excitation
5. intracranial hypertension *
65. What is the pathogenesis of hypertension in some kidney disease?

1. Increase the secretion of adrenaline
2. Increase Renin secretion *
3. increase the secretion of vasopressin from being
4. Increases eritripoietinei secretion
5. increase the secretion of nariuretic hormone
66. Hiperfuncţia bin of the heart which takes place in hypertensive disease?
1. Right ventricle
2. The left Comprise
3. Comprise as
4. The left ventricle *
5. Comprise and right ventricle
68. the endocrine diseases occurs secondary hypertension?

1. Cushing's Disease *
2. primary Hiperaldosteronismul
3. Addison's disease
4. Mixedemul
5. Feocromocitomul *
5. PATHOPHYSIOLOGY OF EXTERNAL RESPIRATION (74)
1. What is hiperpneea?
a. increased respiration
b. * increased respiration amplitudinei
c. decrease in respiration rate
d. decreased respiration amplitudinei
c. increase the minute-breath volume
2. What is polipneea?
a. * increased respiration
b. increasing respiration amplitudinei
c. decrease in respiration rate
3. What is bradipneea?
a. increased respiration
b. increasing respiration amplitudinei
c. * decreased respiration rate
4. What is hiperventilaţia?
a. increasing minute-breath volume
b. decrease the volume-breath minute
c. increased respiration
d. decrease in respiration rate
e. lower respiratory amplitudinei
5. What is hipoventilaţia?
a. increasing minute-breath volume
b. decrease the volume-breath minute
c. increased respiration
d. decrease in respiration rate
e. lower respiratory amplitudinei
6. what changes of composition of the alveolar air is found in the hyperventilation?

a. partial pressure of oxygen below 100 mm Hg
b. partial pressure of oxygen above 100 mm Hg
c. * partial pressure of carbon dioxide less than 40 mm Hg
d. partial pressure of nitrogen under 600 mm Hg
e. partial pressure of nitrogen over 600 mm Hg
7. what changes of composition of the alveolar air is found in hipoventilaţie?
a. * partial pressure of oxygen below 100 mm Hg
b. partial pressure of oxygen above 100 mm Hg
c. partial pressure of carbon dioxide less than 40 mm Hg
d. partial pressure of nitrogen * in 600 mm Hg
e. partial pressure of nitrogen over 600 mm Hg
8. what changes of arterial blood gas composition is found in the hyperventilation?

a. oxygen pressure below 100 mm Hg
b. oxygen pressure above 100 mm Hg
c. * carbon dioxide under pressure of 40 mm Hg
d. the pressure of oxygen above 40 mm Hg
e. nitrogen pressure over 600 mm Hg
9. what changes of gaseous composition of arterial blood is found in the hipoventilaţie?

a. oxygen pressure below 100 mm Hg
b. oxygen pressure above 100 mm Hg
c. carbon dioxide under pressure of 40 mm Hg
d. * the pressure of oxygen above 40 mm Hg
e. nitrogen pressure over 600 mm Hg
10. what changes of acid-base balance is found in the hyperventilation?

a. respiratory acidosis
b respiratory alkalosis.
c metabolic acidosis.
d. metabolic alkalosis
e. balance unchanged
11. what changes of acid-base balance is found in hipoventilaţie?

a respiratory acidosis.
b respiratory alkalosis.
c metabolic acidosis.
d. metabolic alkalosis
e. balance unchanged
12. what changes of ventilatorii parameters of lungs hyperventilation is found in?

a. increases vital capacity of the lungs
b. minute increments-breath volume
c. increase the percentage rate of minute anatomical dead space-the amount of breath
d. * decreases the percentage rate of minute anatomical dead-volume breathing
e. subtract a minute-volume breathing
13. what changes of parameters of ventilatorii of the lungs is found in hipoventilaţie?

a. increases vital capacity of the lungs
b. minute increments-breath volume
c. * percentage rate increases dead space anatomically
d. decreases the percentage rate of the anatomical dead
e. * minute-volume breathing decreases
16. How do I change intratoracică pressure and venous return to the heart in deep breath and
accelerated?
intratoracică pressure increases.
b. * intratoracică pressure drops
c. venous return does not change
d. venous return is difficult
e. * the return of venous blood is facilitated
17. How do I change intratoracică pressure and venous return to the heart breath shallow?
the intratoracică increases the pressure.
b. intratoracică pressure drops
c. venous return does not change
d. * venous return is difficult
e. the return of venous blood is facilitated
18. What is characteristic for shortness of breath?

a. * changing the frequency of respiration
(b). * change the amlitudinei breath
(c). respiration rate change *
(d). changes of blood gas composition
(e). * the subjective sensation of air failure
19. We call Dyspnea inspiratorie?

a. * prolonging inspirului
(b). preliungirea duration of expiratory pressure(peep).
(c). * increased effort inspiring with exhale passively
(d). inspiring effort with increased forced expiration
(e). the extension of inspirului and concomitant expiratory pressure(peep).
20. What is known as Dyspnea expiratorie?

a. extending inspirului
(b). * duration of expiratory pressure(peep) preliungirea
(c). inspiring effort with increased passive expiration
(d). * exhale forcefully
(e). the extension of inspirului and concomitant expiratory pressure(peep).
21. what physical parameters of the alveolar air slows gas diffusion through alveoli-capillary
barrier?
a. partial oxygen pressure increasing
(b). * decreased partial pressure of oxygen
(c). * increased pressure of carbon dioxide
(d). parţialşe pressure drop of carbon dioxide
(e). increasing nitrogen partial pressure
24. what conditions gas diffusion barrier diminishes the alveoli-capillary?

a. * thickening barrier
b. * Interstitial Pulmonary edema
c. atherosclerosis of arteries small circuit
d. hipoperfuzia lungs
e. Air hipobaria
25. what conditions gas diffusion barrier diminishes the alveoli-capillary?

f. * the presence of fluid in the alveoli
g. * reducing the total area of diffusion
h. atherosclerosis of arteries small circuit
i. hipoperfuzia lungs
j. Air hipobaria
26. what condition the gas diffusion barrier diminishes the alveoli-capillary?
k. * thickening barrier
l. atherosclerosis of arteries small circuit
m. hipoperfuzia lungs
n. Air hipobaria
o. airway obstruction aeroconductorii
p. * the presence of fluid in the alveoli
q. atherosclerosis of arteries small circuit
r. hipoperfuzia lungs
s. Air hipobaria
t. airway obstruction aeroconductorii
u. * Interstitial Pulmonary edema
v. atherosclerosis of arteries small circuit
w. hipoperfuzia lungs
x. Air hipobaria
y. airway obstruction aeroconductorii
z. * reducing the total area of diffusion
aa. atherosclerosis of arteries small circuit
bb. hipoperfuzia lungs
cc. Air hipobaria
dd. airway obstruction aeroconductorii
30. what factors reduce the ability of the blood oxigenică?

a. * replacement of the adult hemoglobin, fetal
b. * transforming hemoglobin in methemoglobină
c. decreased concentration in blood serum iron
d. ferritin in the blood decreased concentration
e. transferrin decreased concentration in blood
31. what factors reduce the ability of the blood oxigenică?

f. * reduced hemoglobin content in the blood
g. * Association of carbon monoxide from hemoglobin
h. decreased concentration in blood serum iron
i. ferritin in the blood decreased concentration
j. transferrin decreased concentration in blood
32. what factor decreases the ability of the blood oxigenică?

k. * replacement of the adult hemoglobin, fetal
l. decreased concentration in blood serum iron
m. ferritin in the blood decreased concentration
n. transferrin decreased concentration in blood
o. decreased blood haptoglobinei conentraţiei
p. * reduced hemoglobin content in the blood
q. decreased concentration in blood serum iron
r. ferritin in the blood decreased concentration
s. transferrin decreased concentration in blood
t. decreased blood haptoglobinei conentraţiei
u. * transforming hemoglobin in methemoglobină
v. decreased concentration in blood serum iron
w. ferritin in the blood decreased concentration
x. transferrin decreased concentration in blood
y. decreased blood haptoglobinei conentraţiei
z. * Association of carbon monoxide from hemoglobin
aa. decreased concentration in blood serum iron
bb. ferritin in the blood decreased concentration
cc. transferrin decreased concentration in blood
dd. decreased blood haptoglobinei conentraţiei
36. what hemoglobin decrease compounds oxigenică ability of blood?

a. oxihemoglobina
b. deoxigenată hemoglobin
c. carbohemoglobina
d. * carboxihemoglobina
e. * methaemoglobin
37. what physical and chemical parameters prevents oxygen from hemoglobin pairing in the
circuit
small?
a. * acidosis
b. alkalinization
c. hipocapnia
d. * hipercapnia
e. low temperature
38. what physical and chemical parameters prevents dissociation oxihemoglobinei in the circuit?
a. acidosis
b. * urinary alkalinization
c. * hipocapnia
d. hipercapnia
e. * low-temperature
39. what processes determine pulmonary restriction extraparenchimală?

* diseases of the pleura.
b. * chest diseases
c. disorders of the pulmonary circuit
d. * disorders of neuro-muscular apparatus
e. changes in lung compliance
40. What is known as pulmonary intraparenchimală constraint?

a. * reducing the compliance and elasticity of the lungs
b. reducing the overall compliance of the respiratory system
c. reduce compliance chest
d. reduced compliance of the chest
e. upper airway obstruction
41. What is known as apulmonary bstrucţie?

a. blood flow to their lungs
b. increasing the blood pressure in the pulmonary circuit
c. * increasing resistance of aeroconductoare with pulmonary ventilation malfunction
d. reduction of blood pressure in the pulmonary circuit
c. decreasing the resistance of aeroconductoare
42. what factors can provocă aeroconductorii upper airway obstruction?

a. the presence of thrombi in pulmonary artery
b. *swelling in the lining of the bronchi
c. presence of foreigners in the trachea and bronchi
d. * epilepsy
e. Mediastinal tumors
43. what factors can cause airway obstruction of the lower aeroconductorii?
a. * mucus bronhial hipersecreţia
b. *swelling in the lining of the bronhiolelor terminals
c. the presence of foreigners in the trachea and bronchi
d. epilepsy
e. spasm smooth muscles of? bronchus subsegmentare
44. What are very simple deep breath azuri and accelerated *
a. physical exertion
b. asthma
c. * nerespiratorie acidosis
d. psycho-emotional stress *
e. * circulatory hypoxia
45. What is very simple and breath azuri frequent shallow?

a. hypercapnia
b. pulmonary atelectasis.
c. pulmonary edema
d pneumonia
e. nerespiratorie acidosis
46. in what cases is rare and deep breath?

a. physical exertion
b. * aeroconductorii of stenosis
c. pneumonia
d. pulmonary edema
e. hypoxia of any origin
47. In what case meets expiratorie shortness of breath?

a. pneumonia
b. pulmonary hypertension
c. * asthma
d. the upper aeroconductorii stenosis
e. pulonară atelectasis
48. what biologically tell possesses effect bronhoconstrictor?

a. * histamine
(b). * serotonin
(c). bradykinin
(d). PGF2-Alpha
(e). * acetylcholine
49. what biologically bronchodilator effect possess tell?

a. PGE1
(b). * PGE2
(c). serotonin
(d). prostaciclinele
(e). * PGF2-Alpha
50. what biologically active growing pressure within the pulmonary circuit?
a. * Angiotensin II
(b). serotonin
(c). PGF2-Alpha
(d). PGE1, PGE2
(e). tromboxanul A2
51. what biologically active substances reduce the pressure in the pulmonary circuit?
a. PGI2
(b). Atrial natriuretic Factor
(c). * PGE1, PGE2
(d). serotonin
(e). * bradykinin
52. What factors causes acute respiratory distresul to mature?

a. * total pneumonia
b. * massive blood transfusion
c. systemic hypertension
d. Pulmonary hypertension
e. Portal hypertension
f. Bronhioleleor spasm
53. What factors causes acute respiratory distresul to mature?

g. * various types of shock
h. * disseminated intravasculare coagulation syndrome
i. systemic hypertension
j. Pulmonary hypertension
k. Portal hypertension
l. Bronhioleleor spasm
54. What causes acute respiratory distresul factor to mature?

m. * total pneumonia
n. systemic hypertension
o. Pulmonary hypertension
p. Portal hypertension
q. Bronhioleleor spasm
r. * various types of shock
s. systemic hypertension
t. Pulmonary hypertension
u. Portal hypertension
v. Bronhioleleor spasm
w. * massive blood transfusion
x. systemic hypertension
y. Pulmonary hypertension
z. Portal hypertension
aa. Bronhioleleor spasm
bb. * disseminated intravasculare coagulation syndrome
cc. systemic hypertension
dd. Pulmonary hypertension
ee. Portal hypertension
ff. Bronhioleleor spasm
58. What is pathogenesis of psychological distress in patients acute

respiratory?
a. * trophic disorders of the pulmonary vessels endothelium;
b. * alveoli membrane permeability-capillaries;
c. increasing the flexibility of the lung parenchyma;
d. * fluid extravasation in the alveoli;
e. * formation of hialinice membranes.
59. What is pulmonary edema?

1. accumulation of fluid in the lung interstiţiul
2. accumulation of fluid in the pleural cavity
3. accumulation of fluid in the alveoli
4. accumulation of fluid in the mediastinum
5. the accumulation of fluid in the aeroconductorii
60. What factors causes pulmonary edema?

a. * increase the hydrostatic pressure of the blood in the capillaries and small circulation
b. * increasing the permeability of the vascular wall
c. Pulmonary Hipoperfuzia
d. Vascular shunt right-left
e. Asthma
f. Epilepsy
61. What factors causes pulmonary edema?

g. * block lymphatic drainage of the lung
h. * increased pressure in pulmonary interstiţiul oncotice
i. Pulmonary Hipoperfuzia
j. Vascular shunt right-left
k. Asthma
l. Epilepsy
62. What causes pulmonary edema factor?

m. * increase the hydrostatic pressure of the blood in the capillaries and small circulation
n. Pulmonary Hipoperfuzia
o. Vascular shunt right-left
p. Asthma
q. Epilepsy

r. * block lymphatic drainage of the lung
s. Pulmonary Hipoperfuzia
t. Vascular shunt right-left
u. Asthma
v. Epilepsy
w. * increasing the permeability of the vascular wall
x. Pulmonary Hipoperfuzia
y. Vascular shunt right-left
z. Asthma
aa. Epilepsy
bb. * increased pressure in the interstice oncotice lung
cc. Pulmonary Hipoperfuzia
dd. Vascular shunt right-left
ee. Asthma
ff. Epilepsy
66. Why call lung emphysema?

a. reduction of the lower aeroconductorii tract lumen
b.persistent excessive dilation of the air spaces distal to the Terminal Bronchioles
c. excessive dilatation of pulmonary arterioles
constriction of the lung parenchyma.
e. excessive dilation of the bronchi caliber persistent.
67. That is the main pathogenetic link emfizemului?

a. dizechilibrul of lisosomal proteinases and antiproteinaze with predominance of
antiproteinazelor
(b). * dizechilibrul of lisosomal proteinases and antiproteinaze with predominance of
proteinazelor
(c). * dizechilibrul of trypsin and Alpha 1 antitripsină with predominance of trypsin
(d). dizechilibrul of trpsină and antitripsină with predominance of 1 Alpha Alpha 1
antitripsinei
(e). dizechilibrul of trombogenetici and fibrinolitici in favor of fibrinoliticelor.
68. What are the proteolytic enzyme sources that harm the alveoli?
a. mast cells
(b). * neutrophils
(c). monocyte
(d). * the exocrine pancreas
(e). hepatocitele
69. What is emphysema?

a. increase the residual lung volume
f. * reduction of the vital capacity of the lungs
g. shortness of breath inspiratorie
h. reduction of waste volume
(i). shortness of breath inspiratorie
j. lung hyperventilation
70. What is lung emphysema?

k. * shortness of breath expiratorie
l. * reduction of forced expiratory volume in 1 second
m. shortness of breath inspiratorie
b. reduction of waste volume
it. shortness of breath inspiratorie
p. lung hyperventilation
71. What are lung emphysema?

a. increase the residual lung volume
q. shortness of breath inspiratorie
r. reduction of waste volume
s. shortness of breath inspiratorie
t. lung hyperventilation
72. What is lung emphysema?

u. * reduction of the vital capacity of the lungs
v. shortness of breath inspiratorie
w. reduction of waste volume
x. shortness of breath inspiratorie
y. lung hyperventilation
73. What are lung emphysema?

z. * shortness of breath expiratorie
aa. shortness of breath inspiratorie
bb. reduction of waste volume
cc. shortness of breath inspiratorie
dd. lung hyperventilation
74. What is emphysema?

a. * reduction of forced expiratory volume in 1 second
(b). shortness of breath inspiratorie
(c). reduction of waste volume
(d). shortness of breath inspiratorie
(e). lung hyperventilation
6. PATHOPHYSIOLOGY OF DIGESTIVE AND LIVER (78)

1. what impairs the digestion of pathological processes in oral cavity?
a. hipersalivaţia
b * hiposalivaţia
c. * the lack of salivary amylase
d. lack of lysozyme
e. saliva alkaline reaction
2. What are digestive disorders in the absence of salivary amylase?

the disturbance of the digestion and albumins.
b. digestion disorders dizaharidelor
c. disturbed digestion celulozai
d. the disturbance of digestion of proteins
e. the disturbance of lipid digestion
3. What is hipersalivaţia?
a. * 2,5 L/24 hours
b. 1 l/24 hours
c. 1.5 L/24 hours
d. 0.5 L/24 hours
e. 0,1 L/24 hours
4. What can be the causes of pathological hipersalivaţiei?

a. the teeth eruption in children
b. ingesting dried foods
c. * stomatitele
d. * oral Neoplasms
e. * Parkinson's disease
5. What are the possible consequences of sialoreei?

a. * neutralize gastric juice
(b). lowering the pH of the stomach
(c). * increasing the pH of the stomach
(d). * body dehydration
(e). hipervolemia
6. That is one of the consequences of sialoreei?
f. * neutralize gastric juice
g. Excretory Alkalinization
h. lowering the pH of the stomach
(i). hipervolemia
j. acidity gastric juice

k. * increasing the pH of the stomach
l. Excretory Alkalinization
m. lowering the pH of the stomach
b. hipervolemia
it. acidity gastric juice
p. * body dehydration
q. Excretory Alkalinization
r. lowering the pH of the stomach
s. hipervolemia
t. acidity gastric juice
u. * excretory acidosis
v. Excretory Alkalinization
w. lowering the pH of the stomach
x. hipervolemia
y. acidity gastric juice
10. what causes pathological hiposalivaţiei?

a. * emotional States
(b). * ingestion of food liquids
(c). * dehydration
(d). parotiditele
(e). * salivary ducturilor obstruction
11. what factors exogenous causes poison hipersecreţia?

a. * ethanol
(b). * Hipersecreţia of gastrină
(c). vagotonia *
(d). Hipersecreţia of pepsin
(e). Hipersecreţia colecistokininei
12. what causes poison hipersecreţia exogenous factor?
f. * caffeine
g. Hipersecreţia of pepsin
h. Hipersecreţia colecistokininei
(i). Pancreatic Hipersecreţia
j. Pancreatic Hiposecreţia
k. * ethanol
l. Hipersecreţia of pepsin
m. Hipersecreţia colecistokininei
b. Pancreatic Hipersecreţia
it. Pancreatic Hiposecreţia
p. * nicotine
q. Hipersecreţia of pepsin
r. Hipersecreţia colecistokininei
s. Pancreatic Hipersecreţia
t. Pancreatic Hiposecreţia
15. what endogenous causes poison hipersecreţia factor?
u. * Hipersecreţia of gastrină
v. Hipersecreţia of pepsin
w. Hipersecreţia colecistokininei
x. Pancreatic Hipersecreţia
y. Pancreatic Hiposecreţia
16. what causes endogenous factor hipersecreţia poison?
z. vagotonia *
aa. Hipersecreţia of pepsin
bb. Hipersecreţia colecistokininei
cc. Pancreatic Hipersecreţia
dd. Pancreatic Hiposecreţia
17. How do I change the function of the stomach with hyperacidity hypersecretion?
a. increases the
b. * drops
c. does not change
d. * develop gastric chimostaza
e. develops the dumping syndrome
18. How do I change the intestinal transit in case of hypersecretion with poison hyperacidity?
a. increases the
(b). * drops
(c). does not change
(d). * frequent constipation
(e). diarrhea
19. What is aclorhidria?

a. the absence of Cl ions in the blood
b. * absence of HCl in gastric juice
c. lack of enzymes in gastric juice
d. increased blood pH
e. decreased blood pH
20. What can be the causes of aclorhidriei?

a. * gastrină deficiency
b. * atrophic chronic gastritis
c. * gastric cancer
d. Hypertrophic gastritis
e. gastric ulcer
21. What can be the cause of aclorhidriei?
f. * gastrină deficiency
g. Hypertrophic gastritis
h. gastric ulcer
i. hipersecreţia gastrin
j. pancreatic hipersecreţia
22. What can be the cause of aclorhidriei?

k. * atrophic chronic gastritis
l. Hypertrophic gastritis
m. gastric ulcer
n. hipersecreţia gastrin
o. pancreatic hipersecreţia
23. Which may be due to aclorhidriei?

p. * gastric cancer
q. Hypertrophic gastritis
r. gastric ulcer
s. hipersecreţia gastrin
t. pancreatic hipersecreţia
24. What are the repercussions of HCl in the stomach juice deficiency?
a. growth of intestinal peristaltismului
b. * decreased intestinal peristaltismului
c. maldigestie
d. malabsorption
e. * diarrhea
25. What can be the consequences of vomit incoercibile?

a. hypokalemia
b. Hyperkalaemia
c. * alkalosis
d. acidosis
e. * activation of the Renin-angiotensin-aldosterone
26. What are the causes of insufficient exocrine secretion of the pancreas?
a. * chronic options
b. * pancreatic duct obstruction
c. * simpaticotonia
d. vagotonia
e. duodenal ulcer
27. What is the cause of insufficient exocrine secretion of the pancreas?
f. * chronic options
g. vagotonia
h. duodenal ulcer
i. hioperplazia Alpha cells
j. beta cell hyperplasia

k. * tumors of the pancreas
l. vagotonia
m. duodenal ulcer
n. hioperplazia Alpha cells
o. beta cell hyperplasia
p. * pancreatic duct obstruction
q. vagotonia
r. duodenal ulcer
s. hioperplazia Alpha cells
t. beta cell hyperplasia
u. * simpaticotonia
v. vagotonia
w. duodenal ulcer
x. hioperplazia Alpha cells
y. beta cell hyperplasia
31. What are the consequences of insufficient pancreatic secretion of digestive?

a. * protein maldigestia
b. * maldigestia lipids
c. * maldigestia polysaccharides
d. Maldigestia dipeptidelor
e. Maldigestia of fatty acids
32. What is the consequence of insufficient pancreatic secretion of digestive?
f. * protein maldigestia
g. Maldigestia dipeptidelor
h. Maldigestia of fatty acids
i. Maldigestia dizaharidelor
j. Maldigestia monozaharidelor
33. Which is the consequence of insufficient pancreatic secretion of digestive?
k. * maldigestia lipids
l. Maldigestia dipeptidelor
m. Maldigestia of fatty acids
n. Maldigestia dizaharidelor
o. Maldigestia monozaharidelor
34. What is the consequence of insufficient pancreatic secretion of digestive?
p. * maldigestia polysaccharides
q. Maldigestia dipeptidelor
r. Maldigestia of fatty acids
s. Maldigestia dizaharidelor
t. Maldigestia monozaharidelor
35. What is steatorea?
a. the presence of fat in the blood
b. * removal of excessive fat with masses of feces
c. excessive accumulation of fat in liver parenchyma
d. the Elimination of lipids with urine
e. lack of fat in the masses of feces
36. What can be the causes of steatoreei?

a. * acolia
(b). * pancreatic lipase insufficiency
(c). the shortage of pepsin
(d). colemia
(e). Hyperlipidemia
37. What are acolia?

a. lack of bile in the blood
b. * lack of bile in the intestine
c. the presence of bile in the blood
d. discoloration of faeces
e. lack of bilirubin in the bile
38. what factors causes intestinal maldigestia?

a. the intramural nervous system disorders
b. * inflamato processesаre in the small intestine
c. duodenal ulcer
d. whether duplicate tripsinogenului
e. #atrofia the lining of the small intestine
96. What can be the consequences maldigestiei dizaharidelor?

a. * diarrhea
(b). * dehydration
(c). constipation
(d). hiperhidratare
(e). hypoglycemia
40. What can be the consequences of maldigestiei proteins?

a. * hypoproteinemia
b. * blood plasma hipoonchia
c. * swelling
d. proteinuria
e. immunodeficiencies
41. What is the consequence of protein maldigestiei?
f. * hypoproteinemia
g. proteinuria
h. immunodeficiencies
i. decreasing the concentration of urea in the blood
j. decreasing the concentration of amino acids in the blood
k. * blood plasma hipoonchia
l. proteinuria
m. immunodeficiencies
n. decreasing the concentration of urea in the blood
o. decreasing the concentration of amino acids in the blood
p. * swelling
q. proteinuria
r. immunodeficiencies
s. decreasing the concentration of urea in the blood
t. decreasing the concentration of amino acids in the blood
44. What can be the consequences of maldigestiei lipids?

a. * steatorrhea
b. * blood hipocoagulabilitatea
c. * diarrhea
d. Hyperlipidemia constipation
e. constipation
45. What can be the causes of intestinal autointoxicaţiei?

a. enhancement of decaying processes in the intestine
b. excessive consumption of protein foods
c. * constipaţiile
d. * hepatic insufficiency
e. diarea
46. What are the autointoxicaţiei intestinal manifestations?

a. * hypotension
b. hypertension
c. * headache
d. hypoglycemia
e. hyperglycemia
47. how to change the tone and motility of the stomach in hipoclorhidrie?
a. * hypotonia
b. hipertonus
c. * accelerated evacuaţie
d. chimostaza in the stomach
e. vomiting
48. how to change the tone and motility of the stomach in hiperclorhidrie?
a. hypotonia
b. * hipertonus
c. accelerated evacuaţie
d. * chimostaza in the stomach
e. * vomiting
49. what changes in gastric digestion is found in hipoclorhidrie?

a. maldigestia polysaccharides
b. * protein maldigestia
c. maldigestia lipids
d. improvement of gastric digestion
e. maldigestia pulp
50. what changes in gastric digestion is found in hiperclorhidrie?

b. maldigestia protein
c. maldigestia lipids
d. * relieving gastric digestion
e. maldigestia pulp
51. what changes are found in digestive exocrine pancreas insufficiency?

a. * maldigestia polysaccharides
b. * protein maldigestia
c. * maldigestia lipids
d. improvement of intestinal digestion
e. maldigestia pulp
52. what changes in digestion is found in the secretion of bile insufficiency?

b. * intestinal atonie
c. * steatorrhea
d. amiloree
e. creatoree
53. what changes in digestion is found in the lining of the small intestine?
a. derglarea split polysaccharides
b. * split shifts and dizaharidelor
c. split shifts and modifications
d. * split shifts and dipeptidelor
e. lipid disorders Division
53. the absorption of nutrients which corrupts the affection is the lining of the small intestine?
a. proteins
b. * amino acids
c. dizaharidelor
d. * monozaharidelor
e. water
54. what processes is normally the large intestine affection?
a. split polysaccharides
b. splitting of proteins
c. splitting of lipids
d. the splitting-up of pulp
e. * synthesis of vitamins group B
55. the absorption of the substance which impairs the affection of large intestine?
a. proteins
b. amino acids
c. * mineral salts
d. monozaharidelor
e. * water
56. how to change carbohydrate metabolism in liver failure?

a. * exaggerated hiperlipidemia hyperglycemia
b. * Hypoglycemia on nemâncate
c. fructozemia
d. * lowers the content of glycogen in the liver
e. increases the content of glycogen in the liver
57. How do I change the protein metabolism in hepatic insufficiency?

a. hiperglobulinemia
b. * hipoalbuminemia
c. * hiperaminoacidemia
d. it impairs the synthesis of gamma-globulin level
e. increase the concentration of urea in the blood
58. how to change your metabolism in hepatic lipid?

a. intense lipolysis in the liver
b. * steatosis in the liver
c. * Hyperlipidemia with VLDL
d. * Hyperlipidemia with HDL
e. * Hyperlipidemia with fatty acid neesterificaţi
59. How do I change the biochemistry of blood in hepatic insufficiency?

a. * hiperamoniemia
b. * hipoalbuminemie
c. * hipoprotrombinemie
d. increase the concentration of urea
e. decreases the concentration of ammonia
f. * hiperamoniemia
g. increase the concentration of urea
h. decreases the concentration of ammonia
i. increase the concentration of uric acid
j. increase the concentration of HDL
k. * increase the focus of amino acids aromatizaţi
l. increase the concentration of urea
m. decreases the concentration of ammonia
n. increase the concentration of uric acid
o. increase the concentration of HDL
p. * hipoalbuminemie
q. increase the concentration of urea
r. decreases the concentration of ammonia
s. increase the concentration of uric acid
t. increase the concentration of HDL
u. * hipoprotrombinemie
v. increase the concentration of urea
w. decreases the concentration of ammonia
x. increase the concentration of uric acid
y. increase the concentration of HDL
64. How do I change the biochemistry of blood in cholestasis?

a. * bilirubin, conjugated with hyperbilirubinemia
b. * colalemie
c. * hipoprotrombinemie
d. hyperbilirubinemia with high free
e. Hyperlipidemia
f. * bilirubin, conjugated with hyperbilirubinemia
g. hyperbilirubinemia with high free
h. Hyperlipidemia
i. hiperchilomicronemie
j. increase business aminotransferazelor

k. * hypercholesterolemia
l. hyperbilirubinemia with high free
m. Hyperlipidemia
n. hiperchilomicronemie
o. increase business aminotransferazelor

p. * colalemie
q. hyperbilirubinemia with high free
r. Hyperlipidemia
s. hiperchilomicronemie
t. increase business aminotransferazelor

u. * hipoprotrombinemie
v. hyperbilirubinemia with high free
w. Hyperlipidemia
x. hiperchilomicronemie
y. increase business aminotransferazelor
69. What are the consequences of obturării exeresis duct?
a. * acolia
b. * bilirubin, conjugated with hiperbilirubinemia
c. Hyperlipidemia
d. increase business aminotransferazelor
e. hiperbilirubinemia with high free
70. What are the consequences of obturării exeresis duct?
f. * acolia
g. * maldigestia lipids
h. Hyperlipidemia
71. What are the consequences of obturării hepatic duct?

a. * acolia
b. * bilirubin, conjugated with hiperbilirubinemia
c. Hyperlipidemia
d. increase business aminotransferazelor
e. hiperbilirubinemia with high free
72. What are the consequences of obturării hepatic duct?
f. * acolia
g. * maldigestia lipids
h. Hyperlipidemia
73. what processes of bilirubin metabolism impairs hepatic jaundice is in premicrozomal?

a. * capturing free bilirubin from blood
b. free bilirubin conjugation abstracted from blood
c. excretion of conjugated bilirubin in the bile capillaries hepatocit
d. Tipping the ball through the biliary intrahepatice
e. Tipping the ball through extrahepatic biliary tract
74. what processes of bilirubin metabolism, impairs hepatic jaundice is in microzomal?

a. capturing free bilirubin from blood
b. * free bilirubin conjugation abstracted from blood
75. what processes of bilirubin metabolism impairs hepatic jaundice is in postmicrozomal?

c. * excretion of conjugated bilirubin in the bile capillaries hepatocit
76. what processes of metabolism of bilirubin is normally in intrahepatic mechanic jaundice?

d. * the discharge of bile through the biliary intrahepatice
7. KIDNEY (53)
1. What is the mechanism of pathogenesis of Glomerular hematuriei?

a. #diapedeza erythrocytes through the glomerulus hiperpermeabilizat
b. diapedeza erythrocytes by contorţi proximi miniscule tubules
c. diapedeza through distal contorţi miniscule tubules erythrocytes
d. injury urinary calculi by kidney stones
e. inflammation of the renal bazinetelor
2. What diseases the leucocituria?

a. Urinary #Infecţiile
b. #Pielonefrite
c. #Inflamaţia bladder
d. Glomerulonefrite
e. Acute tubular necrosis
f. Hereditary Tubulopatii
g. Nephrotic syndrome
3. In what condition the leucocituria?
h. Urinary #Infecţiile
i. Glomerulonefrite
j. Acute tubular necrosis
k. Hereditary Tubulopatii
l. Nephrotic syndrome

m. #Pielonefrite
n. Glomerulonefrite
o. Acute tubular necrosis
p. Hereditary Tubulopatii
q. Nephrotic syndrome
r. #Inflamaţia bladder
s. Glomerulonefrite
t. Acute tubular necrosis
u. Hereditary Tubulopatii
v. Nephrotic syndrome
6. What is lipiduria disease?

a. Nephrotic #sindromul
b. nephritic syndrome
c. lipid #degenerescenţe of tubular epithelium
d. hepatic insufficiency
e. hiperlipidemii
7. What factors cause diminishing water in reabsorbţiei renal proximali miniscule tubules?
a. #conţinutul increased osmotic active substances into the primary urine
b. antidiuretic hormone stagnation
c. #distrofia tubular epithelium
d. areactivitatea tubular epithelium at vasopressin
e. inflammation of the renal glomerulilor
8. What factors cause diminishing water in miniscule tubules distal reabsorbţiei and collectors?
(b). #insufucienţa antidiuretic hormone
(c). inflammation of the renal glomerulilor
(d). natriuretic hormone insufficiency
(e). hipersecreţia aldosteronului
a. #distrofia tubular epithelium
(b). #areactivitatea tubular epithelium at vasopressin
(c). inflammation of the renal glomerulilor
(d). natriuretic hormone insufficiency
(e). hipersecreţia aldosteronului
(b). inflammation of the renal glomerulilor
(c). natriuretic hormone insufficiency
(d). hipersecreţia aldosteronului
(e). hipersecreţia Renin
a. #insufucienţa antidiuretic hormone
a. #distrofia tubular epithelium
a. #areactivitatea tubular epithelium at vasopressin
14. What factors cause wasthe fall of the proximal reabsorbţiei of Na ions?
the tubular disorders hereditary.
b. reabsorbţiei disorder of glucose
c. reabsorbţiei disorder of amino acids
d. the shortage of aldosterone
e. hyperaldosteronism
15. What factors cause wasthe fall of itfall reabsorbţiei distal ions Na?
a. # tubulopatii
b. reabsorbţiei disorder of glucose
c. reabsorbţiei disorder of amino acids
d. # shortage of aldosterone
e. hyperaldosteronism
16. The result which is tubular proteinuria disorders?

a. inflammatory #tubulopatii
(b). #tulburări of limfocirculaţiei in kidney
(c). Glomerulonephritis
(d). Urolithiasis
(e). Hydronephrosis
17. The result which is tubular proteinuria disorders?
a. #tubulopatii Dystrophic
(b). #amiloidoza
(c). Glomerulonephritis
(d). Urolithiasis
(e). Hydronephrosis
18. What condition is causing the tubular proteinuria?
a. inflammatory #tubulopatii
(b). Glomerulonephritis
(c). Urolithiasis
(d). Hydronephrosis
(e). nefroscleroza
a. #tubulopatii Dystrophic
(c). Urolithiasis
(d). Hydronephrosis
(e). nefroscleroza
a. #tulburări of limfocirculaţiei in kidney
(c). Urolithiasis
(d). Hydronephrosis
(e). nefroscleroza
a. #amiloidoza
(c). Urolithiasis
(d). Hydronephrosis
(e). nefroscleroza
22. What factors cause wasthe fall of glucose reabsorbţiei?

a. #carenţa hexokinazei in hereditary renal epiteliocitele
(b). glomerulopatii
(c). distal tubulopatii
(d). proximal #tubulopatii
(e). diabetes mellitus
23. what diseases causes aminoacidurie?
a. hereditary hexokinazei deficiency in kidney epiteliocitele

b. glomerulopatii
c. distal hereditary tubulopatii
d. proximal erediatre #tubulopatii
e. # hiperaminoacidemie with liver disease
24. What is hipostenuria disease?

a. diabetes
b. #diabet Insipidus
d. acute Glomerulonephritis
e. dehydration
f. hiperhidratare *
25. the hipostenuria is observed pathologies?

a. diabetes
b. #diabet Insipidus
c. tubular #necroză
d. acute Glomerulonephritis
e. dehydration
26. the hiperstenuria is observed pathologies?

a. #diabet mellitus
b Diabetes Insipidus
c. tubular necrosis
d. #deshidratare
c. hiperhidratare
27. in what cases the izostenuria?
the chronic renal insufficiency.
b. acute glomerulopatii
c. cystitis
d. urethritis
e. hipoaldosteronism
28. what disorder includes nephrotic syndrome?

a. #proteinurie
c # Hyperlipidemia
e. hypertension
f. hipostenurie
d. leucociturie
29. what disorder includes nephrotic syndrome?
b. #hipoalbuminemie
d. #edeme
e. hypertension
f. hipostenurie
g. leucociturie
30. What pathological phenomena includes syndrome nephritic?

a. #hematurie
c. #hipertensiune blood pressure
e. Hyperlipidemia
f. Hyperlipidemia
g. lipidurie
31. What pathological phenomena includes syndrome nephritic?

b. # swelling
d. #oligurie
e. Hyperlipidemia
f. Hyperlipidemia
g. lipidurie
32. what processes cause proximal canaliculară acidosis?
a. H ion secretion disorder
b. reabsorbţiei of #tulburării bicarbonate
c. ammonia reabsorbţiei disorder
d. # administering diuretics-carboanhidrazei inhibitors
c # Fanconi syndrome
33. what processes are causing acidosis distal canaliculară?

a. # H ion secretion disorder
b. reabsorbţiei disorder of bicarbonate
c. ammonia reabsorbţiei disorder
d. administering diuretics-carboanhidrazei inhibitors
c. decrease in glomerular filtration rate as urolithiasis
34. what factors stimulate Renin secretion?

a. # hipoerfuzia renal
b # hyponatriemia associated
c. hiperaldosteronemia
d. hipokaliemia
e. hipernatriemia
35. what factors stimulate Renin secretion?
c. #hipovolemia
d. #simpaticotonia
d. hipokaliemia
e. hipernatriemia
36. what factor stimulates Renin secretion?

a. # hipoerfuzia renal
d. hipokaliemia
e. hipernatriemia
f. hipercalciemia

b # hyponatriemia associated
d. hipokaliemia
e. hipernatriemia
f. hipercalciemia

c. #hipovolemia
d. hipokaliemia
e. hipernatriemia
f. hipercalciemia

d. #simpaticotonia
d. hipokaliemia
e. hipernatriemia
f. hipercalciemia
40. What are endocrine functions of rinichilui?

a. #increţia erythropoietin
b. # paracrină prostaglandin secretion vasodilators
c. increţia of angiotensin
d. enable local system # kalicrein-kinin pathways
e. # increţia of renina
41. What are the causes of acute kidney failure prerenale?
a. severe #hipovolemii
d. compromise of renal artery #
e. renal artery dilation
f. hiperhidratarea
g. hemodiluţia
42. What are the causes of acute kidney failure prerenale?
b. cardiac #insuficienţa with decreasing blood flow
c. #şoc
f. hiperhidratarea
g. hemodiluţia
43. What is the cause of acute kidney failure prerenală?
a. severe #hipovolemii
f. hiperhidratarea
g. hemodiluţia
h. hipoonchia blood plasma
b. cardiac #insuficienţa with decreasing blood flow
f. hiperhidratarea
g. hemodiluţia
c. #şoc
f. hiperhidratarea
g. hemodiluţia
22. What is the cause of acute renal ainsuficienţei prerenală?
d. compromise of renal artery #
f. hiperhidratarea
g. hemodiluţia
46. What is the cause of acute kidney failure intrinsic?

a. # nefrotoxici factors
b. bulk #hemoliză
c # massive necrosis of skeletal muscle
d. constriction of the renal artery
47. what causes insufficiency acute renal postrenal origin?

a. nefrotoxici factors
b. urinary #obstrucţia
c. massive necrosis of skeletal muscle
d. constriction of the renal artery
e. dilation of the renal artery
48. What are the main syndromes in acute renal failure?

a. urinary #sindromul
b. humoral syndrome
c. clinical #sindromul
d. nephrotic syndrome
e. nephritic syndrome
49. What are the manifestations of urinary syndrome of the IRA?

a. #Oligurie
c. #izostenurie
d. #hiposteinurie
e. hematuria
f. hiperstenurie
50. What are the manifestations of the humoral IRA?

a. #hiperazotemie
b. # hiperhidratare
d. #acidoză
e. anemia
f. alkalosis
51. What are the clinical syndrome manifestations in the IRA?

a. nitrogen metabolites retention
b. #dereglări of the respiratory rhythm
c. cardiovascular #dereglari
d. hematologic #tulburări
e. # Neuropsychological disorders
52. What are the causes of chronic kidney failure?

a. primary and secondary Glomerular #Afecţiuni
b. tubulo-interstiliale #afecţiuni
c. renal vascular #afecţiuni
d. severe hipovolemii
b. acute heart failure
53. What is succesivitatea the evolution of acute kidney failure?

the early period, # oligoanurică, poliurică, curing
b. early period, poliurică, oligoanurică, curing
c. early period, compensation, poliurică, insănătoşire
d. early period, oligoanurică, poliurică, uremică.
e. early period, oligoanurică, dismetabolică, uremică, însănătosire.

Pathophysiology: Total Questions-2020 General Pathophysiology: 1448 Special Fiztiopatologia: 572

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Pathophysiology: Total Questions-2020 General Pathophysiology: 1448 Special Fiztiopatologia: 572

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PATHOPHYSIOLOGY:

1. What is the General etiology?

2. (5) The endogenous question serves as a factor of the disease?

4. (2) what effect exercise conditions favourable for the body?

5. (3) what effect exercise conditions unfavorable for the body?

7. What is the General pathogenesis?

8. (2) what is the role of cause in the occurrence of disease?

9. (4) what is the role of conditions in the appearance of the disease?

15. (4) what is the lesion?

1. in all diseases injuries wearing exclusive local character

20. (2) What is the pathogenic factor?

21. What is the chain of causes-effects in the pathogenesis of the disease?

22. What is the main link to the pathogenesis?

23. (1) what is etiotropă therapy of the disease?

24. (4) what is disease pathogenetic therapy?

25. What is symptomatic therapy of the disease?

26. (1) presenting specific prophylaxis of the disease?

27. (2) what is the non-specific disease prophylaxis?

29. (2,3) representing non-specific disease prophylaxis

30. (1) what is the physiological reaction of body feature?

32. (1) what is the physiological reaction of body feature?

35. (1.5) That is characteristic of the physiological reaction of the organism?

1. lower intensity is excitantului

37. (1) the characteristic pathological reaction of the organism?

1. exceeds the force excitantului

38. (1) the characteristic pathological reaction of the organism?

39. (1.5) That is characteristic of pathological reaction of the organism?

40. (1.4) That is characteristic of pathological reaction of the organism?

11. leads to dishomeostazii

41. What is adaptive reaction?

42. These compensatory reaction?

43. What is the reaction of protective?

44. What is the reaction of reparative regulation?

45. (1) Which is the first period of the disease?

49. What is the latent period of the disease?

51. What is full during the disease?

52. (3) what is the resolution of the disease?

55. (3.5) what is the resolution of the disease?

57. What is the pathological process?

58. What are primary mechanisms sanogenetic?

60. What is the cercului vicious in pathogenesis?

2. CELLULAR DAMAGE (167)

2. what is thesecondary insertion points into the cell?

3. How is cellular nonspecific lesions?

4. (2) how to modidfică enzyme spectrum in lobular inflammation, injury of blood?

1. Increased activity of amylase in blood

5. (1) how to modidfică enzyme spectrum in pancreas lesions of blood?

1. Increased activity of amylase in blood

6. (4) how to modidfică enzyme spectrum in lesions of blood miocardiocitului ?

1. Increased activity of amylase in blood

8. What is the effect of mechanical lesion of the cytoplasmic membrane?

15. What is the effect of electric current on the excitable cells?

30. (4.5) What causes cell damage the extracellular dishomeostazii?

67. (3) what is the effect of nonspecific activation of cellular endonucleazelor?

68. (5) what is the effect of nonspecific activation of cellular fosfolipazelor?

69. (4) what is the effect of nonspecific activation of cellular proteazelor?

70. (2) what is the cause of cellular acidosis?

1. activating anaerobic catabolism

72. (1) what is the cause of cellular acidosis?

1. increased intracellular ion Influx of H

1. cellular exacerbation "

74. (3,4) what causes cell acidosis?